Decontamination of SARS-CoV-2 contaminated N95 filtering facepiece respirators using artificial sun lamps.

AIMS: Assess the feasibility of using light from artificial sun lamps to decontaminate N95 filtering facepiece respirators (FFRs) contaminated with SARS-CoV-2. METHODS AND RESULTS: FFR coupons or whole FFRs contaminated with 5 log10 TCID50 (target concentration) SARS-CoV-2 in culture media, simulated saliva, or simulated lung fluid were dried for 1-2 h, then exposed to light from tanning and horticulture lamps to assess decontamination. Exposed coupons and whole FFRs showed SARS-CoV-2 inactivation for all matrices tested. Furthermore, FFRs still met performance specifications after five decontamination cycles. CONCLUSIONS: It is feasible that artificial sunlight from these sun lamps can be used to decontaminate FFRs provided the UV dose is sufficient and the light is unobstructed. Furthermore, decontamination can be performed up to five times without degrading FFR performance. SIGNIFICANCE AND IMPACT OF THE STUDY: This research shows a proof of principle that artificial sun lamps may be an option to decontaminate SARS-CoV-2 on N95 FFRs. UV doses required for inactivation to levels below detection ranged from 4 to 37·8 J cm-2 depending on the light source, virus matrix and FFR type.

Decontamination of SARS-CoV-2 contaminated N95 filtering facepiece respirators (FFRs) with moist heat generated by a multicooker.

Decontamination of N95 filtering facepiece respirators (FFRs) is a crisis capacity strategy allowed when there are known shortages of FFRs. The application of moist heat is one decontamination method that has shown promise and is the approach approved in the Steris Steam Emergency Use Authorization (EUA). This effort examines the use of multicookers to apply moist heat, as they are available in retail stores and more affordable than methods requiring more sophisticated equipment. Four of five multicooker models examined met the acceptance criteria for the test and one model was selected for inactivation testing. Tests were performed on four different FFR models with SARS-CoV-2 suspended in culture media, simulated saliva or simulated lung fluid. Moist heat treatment reduced recoverable titres of SARS-CoV-2 virus to levels below the limit of detection in all tests. Furthermore, these four FFR models showed no loss in collection efficiency, inhalation resistance or visual damage after up to 10 decontamination cycles. Two (2) FFR models showed a slight change in strap elasticity (<9%). These data show that moist heat treatment using a multicooker is a viable option for FFR decontamination in a crisis capacity strategy.

Fluctuations of the tensor order-parameter modes in a cholesteric liquid crystal.

We use a Landau-de Gennes free energy to calculate the fluctuations of the five independent modes of the tensor order parameter for a cholesteric liquid crystal. Our results include, as a limiting case, the two classical director modes, known as the twist mode and the "umbrella" mode. We find, however, in contrast to the classical director model, that there can be substantial temperature dependence to the umbrella mode, as well as three additional modes near the transition to the isotropic phase. We comment on a recent experiment that suggests that two of these additional modes may have already been detected.

Proposal for the temperature-electric-field phase diagram of a ferroelectric smectic-C* liquid crystal.

We report on the results of extensive optical measurements on the ferroelectric smectic-C* phase of the chiral liquid crystal 4-(2(') methyl butyl) phenyl 4(')-n-octylbiphenyl-4-carboxylate. We have explored the entire temperature-electric-field phase space searching for all possible phase transitions in the C* region and have characterized them both as to their character, including whether they are first or second order, and also whether they are of instability or nucleation type. Our results lead us to conclude that the experimental phase diagram is incompatible with all existing theoretical models for the C* phase transitions. We propose instead a phase diagram where two second-order lines and one first-order line meet at a triple point that we tentatively identify as a Lifshitz point.

Immune cells in the corpus luteum: friends or foes?

The corpus luteum produces progesterone, which is essential for the maintenance of pregnancy. In the absence of a viable embryo, the corpus luteum must regress rapidly to allow for development of new ovulatory follicles. In many species, luteal regression is initiated by uterine release of PGF(2alpha), which inhibits steroidogenesis and may launch a cascade of events leading to the ultimate demise of the tissue. Immune cells, primarily macrophages and T lymphocytes, are present in the corpus luteum, particularly at the time of luteolysis. The macrophages are important for ingestion of cellular remnants that result from the death of luteal cells. However, it has also been hypothesized that immune cells are involved directly in the destruction of luteal cells, as well as in the loss of steroidogenesis; this hypothesis is reviewed in the first part of this article. An alternative hypothesis is also presented, namely that immune cells serve to abate an inflammatory response generated by dead and dying luteal cells, in effect, preventing a response that would otherwise damage surrounding ovarian tissues. Finally, the changes in immune cells that accompany maternal recognition of pregnancy and rescue of the corpus luteum are discussed briefly. Inhibition of immune cells in the corpus luteum during early pregnancy may be due to embryonic or uterine signals, or to maintenance of high progesterone concentrations within the luteal tissue.

Repeated exposure to prolactin is required to induce luteal regression in the hypophysectomized rat.

We investigated whether prolactin (PRL) treatments resembling the intermittent PRL surges of estrous cycles could induce luteal regression in hypophysectomized rats. Immature female rats were stimulated to ovulate and form corpora lutea with exogenous gonadotropins, and were hypophysectomized following ovulation. A single s.c. injection of either vehicle (VEH) or PRL was administered to each rat on post-hypophysectomy Day 8 and again on Day 11. The four resulting treatment groups consisted of rats that received two injections of VEH, VEH followed by PRL, PRL followed by VEH, or two injections of PRL. Rats were killed 24 or 72 h following the second injection. Plasma 20alpha-dihydroprogesterone, luteal weight, and total luteal protein were determined. One ovary was sectioned for immunohistochemistry for monocytes/macrophages, apoptotic nuclei, and major histocompatibility class II (MHC II) molecules. No effect of time (following injection) was observed on any endpoint, indicating that PRL does not have an ongoing regressive action. Time groups from within each treatment group were therefore pooled for analysis. Significant declines (P: < 0.05) in plasma concentrations of 20alpha-dihydroprogesterone, luteal weight, and protein per corpus luteum occurred only after two injections of PRL. Numbers of luteal monocytes/macrophages, apoptotic nuclei, and MHC II-positive cells were low in all groups; numbers of luteal monocytes/macrophages increased following two injections of PRL (P: < 0.05). We conclude that PRL has a cumulative regressive effect on the corpus luteum of the hypophysectomized rat. Drawing a parallel with the estrous cycle, we suggest that continued exposure to PRL, over several cycles, is necessary to induce full luteal regression.

Downregulation of long-form prolactin receptor mRNA during prolactin-induced luteal regression.

OBJECTIVE: Prolactin is capable of both trophic and lytic actions in rat corpora lutea. In corpora lutea responding to a trophic prolactin signal, the long form of the prolactin receptor is the dominant form and is upregulated by prolactin. We investigated whether mRNA for the short form of the prolactin receptor was dominant in corpora lutea responding to a lytic prolactin signal, and whether the relative concentrations of the mRNAs for both forms of the prolactin receptor were changed during this response. DESIGN AND METHODS: Immature rats were ovulated by injection of 5 IU equine chorionic gonadotrophin and 5 IU human chorionic gonadotrophin, and were hypophysectomized shortly after ovulation. Nine days after hypophysectomy, rats were injected with prolactin (500 microg/day) or vehicle for 24 (n=6, n=6) or 72 h (n=13, n=5). Total RNA was isolated from corpora lutea and mRNA for both types of prolactin receptor were analyzed by semiquantitative RT-PCR using the ribosomal protein S16 as the internal control. RESULTS: The intensities of the long- and short-form prolactin receptor signals were normalized to the S16 internal control and expressed as relative densitometric units. The normalized values at 24h for prolactin-treated vs vehicle-treated rats were 0.23 +/- 0.05 vs 0.49 +/- 0.15 (P>0.05) for the short form and 4.04 +/- 0.8 vs 4.23 +/- 0. 6 (P>0.05) for the long form. The values for 72 h were 0.30 +/- 0.05 vs 0.24 +/- 0.05 (P>0.05) for the short form and 2.76 +/- 0.4 vs 5. 53 +/- 0.3 (P<0.01) for the long form respectively. CONCLUSION: The long form of the prolactin receptor is the dominant form at both time-points; however, the concentration of mRNA for this receptor isoform was specifically downregulated by prolactin treatment. Our results suggest that the short form of the prolactin receptor alone is unlikely to mediate the luteolytic action of prolactin, but that luteolytic events may be influenced via a change in the ratio of the two receptor isoforms.

Effects of a 3beta-hydroxysteroid dehydrogenase inhibitor on monocyte-macrophage infiltration into rat corpus luteum and on apoptosis: relationship to the luteolytic action of prolactin.

The administration of prolactin to hypophysectomized rats results in regression of the corpora lutea, accompanied by immune-inflammatory events such as infiltration of monocytes and macrophages. Recent reports indicate an autocrine role for progesterone during the lifespan of the corpus luteum. In the present study, an inhibitor of 3beta-hydroxysteroid dehydrogenase, Trilostane, was used to investigate the hypothesis that a decrease in luteal tissue steroids precipitates the cascade of immune-inflammatory events leading to luteal regression in prolactin-treated hypophysectomized rats. Immature rats were induced to ovulate by administering eCG-hCG, and hypophysectomized on the day after ovulation (at 32 days of age). Rats were injected s.c. 9-11 days after hypophysectomy with (a) Trilostane (80 mg kg(-1) day(-1)), (b) ovine prolactin (500 mg day(-1)), (c) Trilostane plus prolactin, or (d) vehicle. Plasma and luteal tissue progesterone and 20alpha-dihydroprogesterone ('progestin') were quantified; luteal tissue monocytes-macrophages and apoptotic nuclei were counted, and luteal wet mass was determined. Rats treated with prolactin alone showed the expected markers of luteal regression: decreased plasma progestin, increased numbers of monocytes-macrophages and apoptotic nuclei in luteal tissue, and decreased luteal wet mass; however, progestin concentration in luteal tissue was unchanged. Treatment with Trilostane reduced plasma and luteal tissue progestin, but did not result in an infiltration of monocytes-macrophages or increased numbers of apoptotic nuclei in the corpora lutea, or any change in luteal wet mass. Trilostane in combination with prolactin reduced plasma and luteal tissue progestin and produced the expected markers of regression, with the exception of luteal tissue mass, which remained unchanged. In conclusion, inhibition of steroidogenesis does not initiate luteal regression or augment prolactin-induced luteal regression in hypophysectomized rats. Prolactin-induced infiltration of monocytes-macrophages is not accompanied by a decrease in luteal tissue progestin, at least in the early stages of luteal regression.

Characterization of the murine BSE infectious agent.

Bovine spongiform encephalopathy (BSE) is a prion-associated disease where the infectious agent is thought to be a host-encoded protein with a protease-resistant conformation (PrP(Sc)). Here, data are presented on the solubilization of purified murine BSE material, using guanidine-HCl as a denaturing agent. This treatment led to loss of infectivity, which was partially recovered on renaturation after dialysis to remove the chaotropic agent. The renatured product was then fractionated on an isopycnic sucrose-density gradient and the fractions were analysed for the presence of PrP(Sc), nucleic acids and infectivity. It was found that the major part of PrP(Sc) (>90%) and the endogenous nucleic acids did not contribute towards the formation of infectious particles on renaturation. Infectivity was distributed in the top three, low-density fractions. Among these, the presence of considerable infectivity in the fraction of lowest density, with barely detectable PrP(Sc), is of particular interest.

The proestrous prolactin surge is not the sole initiator of regressive changes in corpora lutea of normally cycling rats.

During the estrous cycle, secretion of prolactin is largely restricted to a surge on proestrus. We investigated whether this proestrous prolactin surge initiates regression of the corpora lutea of the preceding cycle. Adult rats were killed prior to the prolactin surge (Proestrus group), following the prolactin surge (Estrus group), after chemical blockade of the prolactin surge with bromocryptine (Estrus+BRC group), and after blockade of the prolactin surge and administration of prolactin (Estrus+BRC+PRL group). Corpora lutea of the current (proestrus) or preceding (estrus) cycle were dissected out, weighed, and sectioned for immunohistochemistry or cultured for examination of in vitro progestin production. Numbers of luteal monocytes/macrophages, differentiated macrophages, and apoptotic nuclei per high-power field were greater for Estrus and Estrus+BRC+PRL than for Estrus+BRC, which in turn had greater numbers than Proestrus (P< 0.05). In contrast, BRC completely reversed the decline in luteal weight observed between Proestrus and Estrus (P<0.05). Number of major histocompatibility complex II-positive cells was not different between groups (P>0.05). Finally, progestin production by corpora lutea in vitro was lower for Proestrus than for the other groups (P<0.05). The results indicate that the prolactin surge alone is not responsible for initiation of apoptosis or immune cell infiltration in regressing corpora lutea of the estrous cycle, although prolactin increases these markers of regression. Prolactin does cause a decline in luteal weight; however, the corpora lutea retain the capacity for steroidogenesis. We conclude that although prolactin has a role in luteal regression, it is not solely responsible for the initiation of this process.

Glucocorticoids stimulate the accumulation of lipids in the rat corpus luteum.

We investigated the physiological basis for the trophic effect of glucocorticoids in rat corpora lutea in the absence of pituitary gonadotropins. Immature (Day 29) Sprague-Dawley rats were given eCG and hCG to induce the development of corpora lutea and were hypophysectomized on Day 32. Beginning on Day 40, rats received twice-daily s.c. injections of either dexamethasone (dex; 200 microg/rat/day) or vehicle (controls) and then were killed on Day 44. Plasma 20alpha-dihydroprogesterone, a major steroid produced by the corpora lutea, was higher (p 2-fold of plasma 20alpha-dihydroprogesterone concentration compared to controls. Glucocorticoid receptor protein (about 92 kDa) was detected in both luteal and nonluteal ovarian tissues in this animal model. These effects of glucocorticoids and the presence of the glucocorticoid receptor raise the possibility of a physiological role for glucocorticoids in the rat corpus luteum.

The reproducibility of scrapie-associated fibril and PrPSc detection methods after long-term cold storage of natural ovine scrapie-affected brain tissue.

A pool of grey matter (medulla/brain stem, cerebellum and frontal cerebral cortex) was prepared from the brains of 16 sheep with scrapie, diagnosed clinically and by the demonstration of spongiform encephalopathy. Aliquots from the pool of tissue were finely chopped or homogenized and stored at +4 degrees C or -70 degrees C, after undergoing one of several specific pre-treatments (storage with or without protease inhibitors or, alternatively, with or without the cryoprotectant, dimethyl sulphoxide). At intervals over a period of 2 years, the stored extracts were examined by electron microscopy for the presence of scrapie-associated fibrils (SAFs) and by Western immunoblotting for the disease-specific abnormal protein PrPSc. Throughout the 2-year period, SAFs and PrPSc were detected in the majority of all stored tissue extracts under all combinations of tissue preparation and pre-treatment. The combined detection rates for SAFs and PrPSc were 91% at +4 degrees C and 94% at -70 degrees C. There was no significant difference between the results obtained by the two detection methods and no specific combination of preparation method and pre-treatment was superior to any other. Storage of the samples at -70 degrees C appeared to give better results than storage at +4 degrees C, particularly with regard to fibril detection. For logistical reasons and ease of processing, and to avoid the effects of autolysis on recognizable brain regions, long-term storage at -70 degrees C, without any pre-treatment, would appear to be the method of choice.

Luteal regression in the normally cycling rat: apoptosis, monocyte chemoattractant protein-1, and inflammatory cell involvement.

In hypophysectomized rats, prolactin induces regression of the corpora lutea. Luteal regression is accompanied by infiltration of monocytes/macrophages, declines in luteal mass and plasma progestins, and increased staining for monocyte chemoattractant protein-1 (MCP-1). We investigated whether similar events are induced during the estrous cycle, after the proestrous prolactin surge. Rats were killed on proestrus or on estrus, and one ovary was frozen for immunohistochemical detection of MCP-1, monocytes/macrophages (ED1-positive), and differentiated macrophages (ED2-positive) and for in situ detection of apoptotic nuclei. Corpora lutea of the current (proestrus) or preceding (estrus) cycle were dissected from the ovaries of additional rats and frozen for the same analyses and for determination of total protein content. In sections of whole ovaries, intensity and distribution of MCP-1 staining were increased in corpora lutea of multiple ages on estrus as compared to proestrus, as were numbers of differentiated macrophages and apoptotic nuclei per high-power field. Sections of isolated corpora lutea showed these increases on estrus, and the number of monocytes/macrophages per high-power field was also significantly increased. Accompanying these inflammatory/immune events, the corpora lutea on estrus showed decreased weight and total protein per corpus luteum, as compared to corpora lutea on proestrus. These changes are consistent with a proposed role for prolactin in the initiation of luteal apoptosis and of a sequence of inflammatory/immune events that accompany regression of the rat corpus luteum during the normal estrous cycle.

Molecular screening of sheep for bovine spongiform encephalopathy.

Bovine spongiform encephalopathy (BSE) may have transmitted to sheep through feed and pose a risk to human health. Sheep BSE cannot be clinically distinguished from scrapie, and conventional strain typing would be impractical on a significant scale. As human prion strains can be distinguished by differences in prion protein (PrPsc) conformation and glycosylation we have applied PrP(Sc) typing to sheep. We found multiple Western blot patterns of PrP(Sc) in scrapie, consistent with the known scrapie strain diversity in sheep. Sheep passaged BSE showed a PrP(Sc) banding pattern similar to BSE passaged in other species [Collinge, J., Sidle, K.C.L., Meads, J., Ironside, J. and Hill, A.F., Nature, 383 (1996) 685-690], both in terms of fragment size following proteinase K cleavage and abundance of diglycosylated PrP. However, none of the historical or contemporary scrapie cases studied had a PrP(Sc) type identical to sheep BSE. While more extensive studies, including sheep of all PrP genotypes, will be required to fully evaluate these findings, these results suggest that large scale screening of sheep for BSE may be possible.

Topical anesthesia.

OBJECTIVE: To consider topical anesthetic options available to primary care physicians, indications for their use, and efficacy and safety of these agents as supported by the literature. QUALITY OF EVIDENCE: Five randomized controlled trials were retrieved that compared various topical anesthetics as well as topical anesthetics versus infiltrative anesthesia. MAIN FINDINGS: A combination of lidocaine, epinephrine, and tetracaine (LET) is currently the topical anesthetic of choice for repair of simple lacerations involving the faces and scalps of children. A promising new topical preparation is bupivacaine and epinephrine, but its efficacy must be studied in larger populations before widespread use can be advocated. Using EMLA (eutectic mixture of local anesthetics) for repair of extremity lacerations requires further study and cannot yet be recommended. Continued use of topical tetracaine, adrenaline, and cocaine (TAC) is not supported in the literature, because of its greater expense, its status as a restricted narcotic, its potential for toxicity, and better availability of an equally efficacious alternative, LET. CONCLUSIONS: Children's simple facial and scalp lacerations can be safely repaired using topical LET gel. Physicians must adhere to recommendations to avoid mucous membrane contact and ensure appropriate dosing with these agents. Bupivacaine-epinephrine topical preparation is a promising analgesic agent that warrants further study.

Estrogen withdrawal induces macrophage invasion in the rabbit corpus luteum.

Macrophages within the corpus luteum are associated with spontaneous luteal regression in a number of species. However, an understanding of the consequences of macrophage recruitment on the functional capacity and responsiveness of the luteal tissue has remained elusive. Here we investigate the temporal appearance of macrophages and their potential impact in corpora lutea of rabbits, in which a rapid fall in progesterone synthesis and premature regression of the corpus luteum are initiated by withdrawal of the luteotropic hormone estradiol-17beta. Removal of estradiol implants, placed subcutaneously, induced a significant increase in the average number of macrophages per high-power field (hpf) in corpora lutea (p < 0.05) within 72 h. Replacement of the estradiol implants 48 h after their removal resulted in a marginal rebound of plasma progesterone and a variable number of luteal macrophages (range: 6-160 macrophages/hpf) among the 11 rabbits. A third experiment revealed that the relative numbers of macrophages within the corpora lutea have no apparent relationship to rates of progesterone synthesis in vitro: progesterone production (ng/mg tissue) did not differ (p > 0.05) between corpora lutea of estradiol-maintained rabbits and those of estradiol-replaced rabbits despite obvious differences in numbers of luteal macrophages (2 +/- 1 vs. 42 +/- 10 macrophages/hpf, respectively; p < 0.05). We conclude that the entry/recruitment of macrophages into the rabbit corpus luteum is sensitive to the luteotropic hormone estradiol-17beta and that the presence of macrophages does not preclude the continuation of progesterone production in surviving luteal tissue revitalized after estradiol removal/replacement.

Protein markers in cerebrospinal fluid from BSE-affected cattle.

Two-dimensional gel electrophoresis was used to analyse cerebrospinal fluid (CSF) from 75 suspect cases of bovine spongiform encephalopathy (BSE), 61 of which were confirmed by post mortem brain histopathology, and 38 normal cattle. CSF samples were also examined from cattle killed at periodic intervals through the incubation period following experimental challenge. Consistent changes were recorded in all CSF samples from the confirmed cases of natural BSE and also from cattle showing early signs of experimental disease. The changes consisted of an increased intensity of staining of apolipoprotein E and the presence of two protein spots, as yet unidentified, of molecular weights 35 and 36 kDa, both with a pI of 5.5. These changes were absent in the CSF samples from the normal cattle, from the clinically suspect cattle which were not confirmed as BSE and from the experimentally challenged cattle in the preclinical phase of infection.

Expression of the steroidogenic acute regulatory protein in the corpus luteum of the rabbit: dependence upon the luteotropic hormone, estradiol-17 beta.

The recent characterization of the mitochondrial protein, Steroidogenic Acute Regulatory (StAR) protein, as a rate-limiting protein in steroidogenesis prompted us to investigate whether StAR is expressed in the rabbit corpus luteum and whether the expression of StAR is responsive to estradiol-17 beta, the luteotropic hormone in the rabbit. In rabbits treated continuously with exogenous estradiol through Day 13 of pseudopregnancy (n = 9), immunoblot analysis revealed that luteal expression of StAR was stable, ranging from 8.5 to 9.7 U of corrected integrated optical density. Plasma progesterone concentration (mean +/- SEM) remained elevated in these rabbits (14.3 +/- 2.1 ng/ml). In contrast, expression of StAR decreased in corpora lutea of rabbits deprived of estradiol for the last 48 and 72 h of the experiment (4.9 +/- 2.2 and 0.3 +/- 0.2 U, respectively, n = 3 per group), and was associated with a decline in plasma progesterone (0.8 +/- 0.1 and 0.5 +/- 0.3 ng/ml, respectively). Replacement of estradiol after 48 h of estradiol deprivation (n = 3) stimulated the reappearance of StAR (10.3 +/- 2.6 U) and the restoration of plasma progesterone (10.4 +/- 4.9 ng/ml). [35S]Methionine labeling of proteins in rabbit corpora lutea revealed that several isoforms of StAR protein were specifically synthesized in response to estradiol treatment. Collectively, these observations are consistent with a proposed role for StAR in the mediation of the luteotropic effect of estrogen to promote the synthesis of progesterone in the rabbit.

Prolactin-induced regression of the rat corpus luteum: expression of monocyte chemoattractant protein-1 and invasion of macrophages.

Monocyte chemoattractant protein-1 (MCP-1) is a potential mediator of the recruitment of monocytes/macrophages into the regressing corpus luteum (CL). We investigated whether the luteolytic effect of prolactin in the rat is associated with the expression of MCP-1 and an invasion of monocytes/macrophages. Ovulation was induced in immature female rats by injection of eCG (5 IU, s.c.) at 30 days of age. All rats were hypophysectomized 3 days later. Rats received injections of ovine prolactin (250 micrograms, s.c.) at 12-h intervals on Day 9, 10, and 11 posthypophysectomy; controls received injection of vehicle. Rats were killed by decapitation 24, 48, or 72 h after the first injection of prolactin or vehicle. In rats treated with prolactin, immunoreactive MCP-1 was detected in the CL at 24 h after the first injection, and a consistent level of staining was reached by 72 h with immunodetectable MCP-1 diffused throughout individual CL. The number of monocytes/macrophages in the CL (mean +/- SEM) increased significantly after prolactin treatment, from 3.1 +/- 1.8 at 24 h to 49.3 +/- 8.2 at 72 h (p < 0.05), and the number of monocytes/macrophages was different from that in control, vehicle-treated rats at 72 h (10.3 +/- 4.1; p < 24 and 72 h in prolactin-treated rats (p < 0.05). It is concluded that a potentially important component of the luteolytic effect of prolactin in the rat is the expression of MCP-1 and invasion of monocytes/macrophages into the CL.

Expression of monocyte chemoattractant protein-1 in the corpus luteum of the rat.

The known accumulation of macrophages in corpora lutea (CL) at the time of luteal regression prompted us to investigate whether the chemoattractant protein monocyte chemoattractant protein-1 (MCP-1) is expressed in the rat CL. On the day of confirmed mating (Day 0 of pregnancy), regressing CL from the previous (nonfertile) estrous cycle contained immunodetectable MCP-1 and numerous monocytes/macrophages, whereas the newly formed CL of pregnancy, within the same ovary, contained little MCP-1 and few monocytes/macrophages. MCP-1 diminished in the regressing CL on Days 3 and 9 of pregnancy, although numerous monocytes/macrophages remained. The CL of pregnancy on Days 3 and 9 of pregnancy contained minimal MCP-1 and relatively few monocytes/macrophages. By Days 17 and 21 of pregnancy, however, prior to parturition and prior to an accumulation of monocytes/macrophages, expression of MCP-1 increased in the CL of pregnancy. Northern blots revealed a resurgence of luteal MCP-1 mRNA on Day 21 of pregnancy: 3805 +/- 1077 on Day 21 vs. 1059 +/- 177 on Day 9 (p < 0.05; expressed as densitometric units relative to beta-actin). In conclusion, the expression of MCP-1 in the rat CL in association with, or preceding, the appearance of monocytes/macrophages at the time of luteal regression is consistent with the known role of MCP-1 as a potent chemoattractant for monocytes/macrophages. This suggests that MCP-1 might have a prominent role in the immunological process of luteal regression.