Possible Hematological Changes Associated with Acute Gastroenteritis among Kindergarten Children in Gaza.

BACKGROUND: Gastroenteritis is considered one of the leading causes of morbidity and mortality in children especially in developing countries. It is a major childhood problem in Gaza and one of the most common etiologic agents of iron deficiency anemia (IDA). AIM: This study was conducted to investigate possible changes in blood parameters that are associated with gastroenteritis infection among kindergarten children in Gaza. SUBJECTS AND METHODS: A cross-sectional case-control study was performed including kindergarten children suffering from gastroenteritis and matched healthy control group. Types of etiological agents were identified using standard microbiological and serological procedures. Blood samples were collected for estimation of complete blood count and for determination of serum iron, total iron binding capacity (TIBC), and transferrin saturation. Independent sample t-test was used for comparisons and performed using SPSS software version 17(Chicago Illinois USA). RESULTS: The prevalence of enteric pathogens among cases (88.5% [85/96]) was significantly higher than in asymptomatic controls (11.1% [6/54]). The most common enteric pathogens isolated were Entamoeba histolytica (28% [42/91]) and Giardia lamblia (26.7% [40/91]). Blood tests revealed that 21.8% (21/96) of cases and 14.8% (8/54) of controls had IDA, which were not significantly different. Meanwhile, a significant difference was found between the TIBC and hemoglobin in cases compared to controls. CONCLUSION: This study indicates that gastroenteritis infection could be considered as a common health problem in kindergarten children in Gaza, and it is possibly associated with changes in hemoglobin concentration and TIBC.

Possible risk factors associated with burn wound colonization in burn units of Gaza strip hospitals, Palestine.

The epidemiological pattern and risk factors of burns and burn infections varies widely in different parts of the world. This study aims to determine the epidemiologic pattern of burn injuries and possible risk factors associated with burn infections in burn units of Gaza strip hospitals. A total of 118 patients were included in the study. The data collected included: patient age and gender, the causes, site, degree, and TBSA of the burns, as well as surgical operations, length of hospital stay, and microbiological profile of samples collected from patients, the environment, and from health care staff. Pediatric and adult patients accounted for 72% and 28% respectively. 58.5% of all patients were male and 41.5% were female. The most common etiological factors in children were scalding, while in adults these were open fire and flammable liquids. The mean TBSA was 12% with a range from 1-90%. Second and third degree burns accounted for 78% and 22% respectively. The area of the body most often affected was the torso (39%), followed by the lower limb (29.7%), and upper limb (17.8%). The predominant microorganisms isolated from burn wounds were Pseudomonas aeruginosa, Enterobacter spp. and Staphylococcus spp. The study showed the highest risk groups to be children and males, and enabled us to identify possible risk factors that can help in future efforts toward prevention and minimizing nosocomial infections in burn units of Gaza strip hospitals.

Le profil épidémiologique et les facteurs de risque des brûlures et des infections de brûlures varient considérablement dans différentes parties du monde. Cette étude vise à déterminer le profil épidémiologique des brûlures et des facteurs de risque possibles associés aux infections de brûlures dans les unités de soins aux brûlés dans les hôpitaux de la bande de Gaza. Un total de 118 patients ont été inclus dans l'étude. Les données recueillies comprennent: l'âge et le sexe du patient, les causes, le site, et le degré TBSA des brûlures, ainsi que les opérations chirurgicales, la durée du séjour à l'hôpital, le profil microbiologique des échantillons prélevés sur les patients, sur l'environnement et sur le personnel de soins de santé. Les patients pédiatriques et adultes représentaient 72% et 28% respectivement. 58,5% des patients étaient des hommes et 41,5% étaient des femmes. Les facteurs étiologiques les plus courants chez les enfants ont été échaudage, tandis que chez les adultes s'agissait feu ouvert et liquides inflammables. Le TBSA moyenne était de 12% avec un intervalle de 1% à 90%. Les brûlures au deuxième et troisième degré représentaient 78% et 22% respectivement. La zone du corps la plus souvent touchée était la torse (39%), suivi par le membre inférieur (29,7%), et du membre supérieur (17,8%). Les micro-organismes prédominants isolés des brûlures étaient Pseudomonas aeruginosa, Enterobacter spp. et Staphylococcus spp. Selon cette étude, les groupes les plus à risque seraient les enfants et les hommes. En plus, cette étude nous a permis d'identifier les facteurs de risque possibles, et ces informations peuvent aider dans les efforts futurs vers la prévention et la réduction des infections nosocomiales dans les unités de soins aux brûlés de la bande de Gaza.

Possible health effects of liquefied petroleum gas on workers at filling and distribution stations of Gaza governorates.

Liquefied petroleum gas (LPG) is widely used in the Gaza Strip for domestic purposes, in agriculture and industry and, illegally, in cars. This study aimed to identify possible health effects on workers exposed to LPG in Gaza governorates. Data were collected by a questionnaire interview, and haematological and biochemical analyses of venous blood samples were made from 30 workers at filling and distribution stations and 30 apparently healthy controls. Statistically significant differences were found in all self-reported health-related complaints among LPG workers versus controls. LPG workers had significantly higher values of red blood cell counts, haemoglobin, haematocrit mean corpuscular haemoglobin and platelet counts. They also had significantly higher values of kidney function tests (urea, creatinine and uric acid) and liver function enzyme activities (aspartate aminotransferase and alanine aminotransferase). LPG workers at Gaza Strip petroleum stations are at higher risk for health-related symptoms and clinical abnormalities.

Possible health effects of liquefied petroleum gas on workers at filling and distribution stations of Gaza governorates

Liquefied petroleum gas [LPG] is widely used in the Gaza Strip for domestic purposes, in agriculture and industry and, illegally, in cars. This study aimed to identify possible health effects on workers exposed to LPG in Gaza governorates. Data were collected by a questionnaire interview, and haematological and biochemical analyses of venous blood samples were made from 30 workers at filling and distribution stations and 30 apparently healthy controls. Statistically significant differences were found in all self-reported healthrelated complaints among LPG workers versus controls. LPG workers had significantly higher values of red blood cell counts, haemoglobin, haematocrit mean corpuscular haemoglobin and platelet counts. They also had significantly higher values of kidney function tests [urea, creatinine and uric acid] and liver function enzyme activities [aspartate aminotransferase and alanine aminotransferase]. LPG workers at Gaza Strip petroleum stations are at higher risk for health-related symptoms and clinical abnormalities

Elevated interleukin-8 concentrations in cervical secretions are associated with preterm labour.

The aim of this study was to assess the potential clinical utility of interleukin-8 (IL-8) present in cervical secretions as a marker of preterm labour and delivery. Samples of cervical mucus from 91 pregnant women were assessed for the presence and concentration of IL-8. Two samples were collected (at 18 +/- 2 and 28 +/- 2.5 weeks of gestation) and correlated with cervicovaginal microbiology and cervical length, as measured by transvaginal ultrasound. The IL-8 concentration at 28/40 was significantly higher in women who went on to deliver preterm (p < 0.01), and there was a greater than five-fold increase from 18 to 28 weeks in 6/7 of these women.

Quantitative and qualitative influences of tapasin on the class I peptide repertoire.

Tapasin is critical for efficient loading and surface expression of most HLA class I molecules. The high level surface expression of HLA-B*2705 on tapasin-deficient 721.220 cells allowed the influence of this chaperone on peptide repertoire to be examined. Comparison of peptides bound to HLA-B*2705 expressed on tapasin-deficient and -proficient cells by mass spectrometry revealed an overall reduction in the recovery of B*2705-bound peptides isolated from tapasin-deficient cells despite similar yields of B27 heavy chain and beta(2)-microglobulin. This indicated that a proportion of suboptimal ligands were associated with B27, and they were lost during the purification process. Notwithstanding this failure to recover these suboptimal peptides, there was substantial overlap in the repertoire and biochemical properties of peptides recovered from B27 complexes derived from tapasin-positive and -negative cells. Although many peptides were preferentially or uniquely isolated from B*2705 in tapasin-positive cells, a number of species were preferentially recovered in the absence of tapasin, and some of these peptide ligands have been sequenced. In general, these ligands did not exhibit exceptional binding affinity, and we invoke an argument based on lumenal availability and affinity to explain their tapasin independence. The differential display of peptides in tapasin-negative and -positive cells was also apparent in the reactivity of peptide-sensitive alloreactive CTL raised against tapasin-positive and -negative targets, demonstrating the functional relevance of the biochemical observation of changes in peptide repertoire in the tapasin-deficient APC. Overall, the data reveal that tapasin quantitatively and qualitatively influences ligand selection by class I molecules.

Distinct functions of tapasin revealed by polymorphism in MHC class I peptide loading.

Peptide assembly with class I molecules is orchestrated by multiple chaperones including tapasin, which bridges class I molecules with the TAP and is critical for efficient Ag presentation. In this paper, we show that, although constitutive levels of endogenous murine tapasin apparently are sufficient to form stable and long-lived complexes between the human HLA-B*4402 (B*4402) and mouse TAP proteins, this does not result in normal peptide loading and surface expression of B*4402 molecules on mouse APC. However, increased expression of murine tapasin, but not of the human TAP proteins, does restore normal cell surface expression of B*4402 and efficient presentation of viral Ags to CTL. High levels of soluble murine tapasin, which do not bridge TAP and class I molecules, still restore normal surface expression of B*4402 in the tapasin-deficient human cell line 721.220. These findings indicate distinct roles for tapasin in class I peptide loading. First, tapasin-mediated bridging of TAP-class I complexes, which despite being conserved across the human-mouse species barrier, is not necessarily sufficient for peptide loading. Second, tapasin mediates a function which probably involves stabilization of empty class I molecules and which is sensitive to structural compatibility of components within the loading complex. These discrete functions of tapasin predict limitations to the study of HLA molecules across some polymorphic and species barriers.

Interleukin-8 release from human gestational tissue explants: effects of gestation, labor, and chorioamnionitis.

Interleukin-8 (IL-8) is a chemotactic cytokine that has been implicated in the process of human parturition, including the processes of cervical ripening and rupture of fetal membranes. In this study, the in vitro release of IL-8 from human amnion, choriodecidua, and placenta tissues obtained before and after spontaneous labor onset both at term and preterm, was assessed. The effect of chorioamnionitis on IL-8 release was also established. All tissue explants examined released IL-8; however, IL-8 release from choriodecidual explants was significantly (p < 0.02) greater than that observed from amnion and placenta. Furthermore, choriodecidual IL-8 release was significantly (p < 0.001) greater from term tissues (850 +/- 134.4 ng/mg DNA, n = 18) than from preterm tissues (458 +/- 68.8 ng/mg DNA, n = 17). Spontaneous onset of labor, irrespective of the eventual mode of delivery, was not associated with any significant changes in IL-8 release from human gestational tissues compared to not-in-labor tissues, both at term and preterm. IL-8 release from gestational tissues was not significantly different in the absence or presence of chorioamnionitis. These data are in contrast to the previously reported stimulatory effects of bacterial endotoxin on IL-8 release from human gestational tissues. The data are consistent, however, with the suggestion that IL-8 release is an early event in chorioamnionitis that precedes the appearance of clinically overt symptoms.

Interleukin-8 release from human gestational tissue explants: the effects of lipopolysaccharide and cytokines.

Interleukin (IL)-8 is a chemotactic cytokine that has been implicated in the etiology of infection-induced and normal human labor. In particular, IL-8 has been implicated in the processes of cervical ripening and rupture of fetal membranes because of its role in neutrophil activation and release of cellular matrix remodeling enzymes. In this study, we tested the hypotheses that IL-8 is released locally in the intrauterine environment from human amnion, choriodecidua, and placenta, and that IL-8 release from these tissues is increased by bacterial endotoxin, lipopolysaccharides (LPS), and inflammatory cytokines. IL-8 was released from human amnion, choriodecidual, and placental explants, with choriodecidua demonstrating the most abundant release. IL-8 release was significantly (multiple analysis of variance, p < 0.05) increased by LPS in a time- and dose-dependent manner from both choriodecidual and placental explants, but not from amnion explants. In addition, IL-1alpha (0.28 nM) and tumor necrosis factor alpha (TNFalpha, 10 nM) significantly (Student's t-test, p < 0.05) increased IL-8 release from placental explants 2- to 3-fold. These studies establish that the amnion, choriodecidua, and placenta are a source of IL-8 and demonstrate tissue-specific and differential regulation of IL-8 release by LPS, IL-1alpha, and TNF-alpha. These data support a role for IL-8 in a cascade of inflammatory events initiated by an intrauterine infection and resulting in activation of the labor process.

Tumor necrosis factor-beta in human pregnancy and labor.

The aims of this study were to determine tumor necrosis factor-beta (TNF-beta) concentration profiles in peripheral venous plasma and amniotic fluid during pregnancy and at the time of labor and to characterise TNF-beta mRNA expression and TNF-beta release from human gestational tissues. In addition, we investigated the expression of TNF-beta binding protein, lymphotoxin-beta (LT-beta), in human gestational tissues. The mean (+/-S.E.M.) TNF-beta concentrations in maternal plasma (TIL, 78 +/- 12 pg/ml, n = 7 vs. TNIL, 304 +/- 88 pg/ml, n = 7) and amniotic fluid (TIL, 8 +/- 5 pg/ml, n = 6 vs. TNIL, 73 +/- 20 pg/ml, n = 20) were significantly (P < 0.05) decreased in association with term labor-onset (TIL) compared to term not-in-labor (TNIL). TNF-beta concentration in maternal plasma and amniotic fluid did not change significantly either with preterm labor (PIL), or during pregnancy. Group-matched comparison of maternal plasma and amniotic fluid TNF-beta concentrations demonstrated that amniotic fluid TNF-beta concentrations were 6-8 fold lower than maternal plasma TNF-beta concentrations. Furthermore, no detectable TNF-beta was secreted from cultured human amniotic, choriodecidual and placental explants. Although, TNF-beta mRNA was detected in amnion, choriodecidual and placenta, LT-beta was similarly expressed in these tissues, suggesting that TNF-beta may be cell membrane bound. These data demonstrate that TNF-beta is present at low levels within the intrauterine environment and may suggest that TNF-beta is specifically inhibited at the maternal-fetal interface.

Labour-associated increase in interleukin-1 alpha release in vitro by human gestational tissues.

The aims of this study were to investigate the concentration and release of interleukin-1 alpha (IL-1 alpha) at the time of human term labour, and to study the regulation of IL-1 alpha release from human gestational tissue explants by bacterial endotoxin. Immunoreactive IL-1 alpha concentrations in maternal plasma, amniotic fluid and conditioned media from human amniotic fluid and conditioned media from human amniotic, choriodecidual and placental explants were quantified before and after spontaneous term labour-onset and delivery. Furthermore, the effects of a bacterial endotoxin, lipopolysaccharide (LPS), on the release of IL-1 alpha from human gestational tissue explants over a time course of 24 h (n = 3) and LPS concentrations ranging from 10-10(7) pg/ml (n = 3) were investigated. IL-1 alpha concentrations in maternal plasma and amniotic fluid did not change significantly with spontaneous term labour-onset. In contrast, IL-1 alpha was released in detectable amounts from human amniotic and choriodecidual explants only in association with term labour-onset and delivery. Similarly, placental release of IL-1 alpha was increased significantly in explant cultures in association with term labour-onset and delivery. LPS increased IL-1 alpha release significantly only from human placental explants from both term not-in-labour and term after-labour tissues. The data demonstrate differential regulation of IL-1 alpha release from human gestational tissues in association with labour and LPS treatment and the observations support the hypothesis that the labour-associated increase in IL-1 alpha release from the fetal membranes is independent of exposure to bacterial endotoxin.

Differential release of interleukin-6 from human gestational tissues in association with labour and in vitro endotoxin treatment.

In this study, we quantified interleukin-6 (IL-6) concentrations in amniotic fluid at term and preterm labour, and determined the gestational tissue source of IL-6. In addition, aspects of the regulatory mechanisms involved in IL-6 release at the time of term labour and in response to bacterial endotoxin, lipopolysaccharide (LPS), have been established. IL-6 concentrations were 2-fold higher in amniotic fluid collected at term compared with preterm gestation, with an additional 2-fold increase in association with term labour. IL-6 was released from all choriodecidual and placental explants but was detected in only 33% of amniotic explant cultures of tissues obtained before labour onset. In contrast, IL-6 was detected in all amniotic, choriodecidual and placental cultures of tissues obtained after term labour onset and delivery, and the mean IL-6 release was significantly higher than that measured in explant cultures of both amniotic (80-fold increase, P < 0.0001) and choriodecidual (3-fold increase, P < 0.02) but not placental explants taken at the time of elective Caesarean section at term before labour onset. LPS significantly (P < 0.05) increased the release of IL-6 from human choriodecidual and placental explants but not amniotic explants, in a time- and dose-dependent manner. IL-6 is a physiological constituent of amniotic fluid and its production by gestational tissues is differentially regulated by LPS and spontaneous labour onset and delivery.

Cellular localization and steroid hormone regulation of mRNA encoding tumour necrosis factor receptor I in mouse uterus.

Signals transduced by binding of tumour necrosis factor alpha (TNF) and lymphotoxin alpha (LT-alpha) trimers to high-affinity cell membrane receptors, TNF-RI (p55/p60) and TNF-RII (p75/p80), affect many cell functions. In this study, expression of the gene encoding TNF-RI in uteri of cyclic mice was mapped using in situ hybridization. TNF-RI hybridization signals fluctuated during the cycle. Signal intensity was highest during dioestrus-II, when mRNA encoding TNF-RI was present in endometrial epithelial and stroma cells, as well as in myometrial smooth muscle and connective tissue cells. The ability of oestradiol and progesterone to modulate steady state concentrations of mRNA encoding TNF-RI in uterine cells was assessed by using in situ and northern blot hybridization procedures. Seven days after ovariectomy, low concentrations of mRNA encoding TNF-RI were detected by northern analysis and weak in situ hybridization signals were identified in epithelia and some myometrial connective tissue cells. Administration of oestradiol, progesterone or oestradiol plus progesterone to ovariectomized animals stimulated temporal and cell type-specific changes in steady state concentrations of mRNA encoding TNF-RI that were unique to each hormonal regimen. Maximal induction of mRNA encoding TNF-RI required 24 h of oestradiol stimulation and 72 h of progesterone stimulation. In uteri treated with oestradiol plus progesterone, the oestradiol pattern predominated over the progesterone pattern. Thus, multiple cell types in cyclic mouse uteri express the gene encoding TNF-RI, and expression in specific cells is controlled by female steroid hormones.

Expression and localization of messenger RNA for tumor necrosis factor receptor (TNF-R) I and TNF-RII in pregnant mouse uterus and placenta.

The temporal and cell-specific localization of tumor necrosis factor (TNF) receptor mRNAs in the uterus and placenta during pregnancy in the mouse was investigated. Messenger RNA for TNF and the TNF receptors (TNF-RI, p55/p60 and TNF-RII, p75/p80) was assessed by northern blot andin situ hybridization. TNF, TNF-RI and TNF-RII specific transcripts were present on days 7 through 18 of pregnancy. Relative concentrations of TNF mRNA decreased from days 7 to 18 with levels being higher in the uterus than the placenta. In contrast TNF-RI mRNA levels were constant throughout gestation and no differences were seen between steady state levels in the uterus and placenta. Two transcripts for TNF-RII (3.6 and 4.5 kb) were identified in all tissues. Steady state levels of TNF-RII mRNA increased throughout gestation and levels were higher in the placenta than in the uterus. On day 9 of gestation, TNF-RI and TNF-RII mRNAs were localized to undecidualized endometrium, mesometrial decidual cells, and the developing placenta. In addition, muscle cells contained TNF-RI but not TNF-RII mRNA. By day 15 of gestation, TNF-RI and TNF-RII transcripts were primarily localized to the uterine epithelium and trophoblast giant cells and spongiotrophoblast cells in the placenta. The results of these studies reveal the uterine and placental cell-specific expression of TNF receptor mRNAs during pregnancy in the mouse and provide insight into the cellular targets of TNF action.

Tumour necrosis factor alpha during human pregnancy and labour: maternal plasma and amniotic fluid concentrations and release from intrauterine tissues.

The aims of this study were: to quantify immunoreactive tumour necrosis factor alpha (TNF-alpha) concentrations in maternal plasma and amniotic fluid obtained from women during pregnancy and labour, both at term and preterm; and to establish the effects of bacterial endotoxin and cytokines on the in vitro release of TNF-alpha from intrauterine tissues. Maternal plasma TNF-alpha concentrations did not change during pregnancy (457.2 +/- 102.9 ng/l, mean +/- SEM, N = 52) or at the time of labour (543.5 +/- 138.6 ng/l, N = 43). In contrast, amniotic fluid TNF-alpha concentrations increased significantly (p < 0.05) during pregnancy (early pregnancy, EP, 93.0 +/- 24.8 ng/l, N = 7; preterm not-in-labour, PNIL, 186.8 +/- 42.9 ng/l, N = 16; term not-in-labour. TNIL, 499.7 +/- 150.9 ng/l, N = 13) and in association with preterm labour (preterm in-labour, PIL, 958.7 +/- 575.6 ng/l, N = 5 vs PNIL, 186.8 +/- 42.9 ng/l, N = 16). Choriodecidual and placental explants (N = 3) maintained in in vitro culture released TNF-alpha. Furthermore, the release of TNF-alpha was increased significantly (p < 0.05) by bacterial endotoxin (lipopolysaccharide, 10 ng/l-10 mg/l) but was not affected by the following cytokines at the indicated doses: interleukin-1 alpha (0.28 nmol/l), interleukin-6 (12.5 nmol/l), granulocyte colony-stimulating factor (2.5 nmol/l), granulocyte-macrophage colony-stimulating factor (35 nmol/l), macrophage colony-stimulating factor (1.2 nmol/l), leukaemia inhibitory factor (0.45 nmol/l) and transforming growth factor-beta (0.4 nmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Leukemia inhibitory factor: association with intraamniotic infection.

OBJECTIVE: Our purpose was to investigate whether leukemia inhibitory factor is associated with intraamniotic infection. STUDY DESIGN: A comparative clinical study of amniotic fluid leukemia inhibitory factor concentrations was performed. RESULTS: Leukemia inhibitory factor was undetectable (< 1 ng/ml) by radioreceptor assay during normal pregnancy at midtrimester and at term. Among women in labor those with intraamniotic infection had higher leukemia factor concentrations than those without infection before term (p < 0.001) and at term (p < 0.005). The leukemia inhibitory factor concentrations correlated with the amniotic fluid white blood cell counts (r = 0.47) (p < 0.001). In cultured human gestational tissue explants, leukemia inhibitory factor release was significantly enhanced by endotoxin, interleukin-1 alpha, and tumor necrosis factor-alpha however, leukemia inhibitory factor did not enhance the release of prostaglandin E2 by these tissues. CONCLUSIONS: Amniotic fluid leukemia inhibitory factor concentrations were elevated during intraamniotic infection and gestational tissues released leukemia inhibitory factor in response to bacterial products and inflammatory mediators.

Interleukin 8 concentrations in amniotic fluid and peripheral venous plasma during human pregnancy and parturition.

To establish the gestational and labour-associated changes in interleukin 8 (IL-8) release, we have determined the concentration of this cytokine in maternal peripheral plasma and amniotic fluid from 15 weeks of gestation to term and in association with spontaneous-onset labour at term and preterm. No statistically significant changes in peripheral plasma IL-8 concentration were observed during pregnancy or in association with labour onset (mean concentration 56.5 +/- 14.5 ng/l, N = 64). The IL-8 concentrations in amniotic fluid were up to 50-fold greater than those observed in peripheral plasma (p < 0.05) and increased significantly (p < 0.05) during pregnancy. At term, but before the onset of labour, amniotic fluid concentrations of IL-8 averaged 969.2 +/- 553.5 ng/l (N = 12). In association with labour at term, IL-8 concentrations increased to 3895.8 +/- 1414.4 ng/l (N = 6, p < 0.03). The concentration of IL-8 in amniotic fluid obtained from women in preterm labour averaged 1854.7 +/- 1352.6 ng/l (N = 6) but was not statistically different from the concentration of IL-8 in amniotic fluid obtained from gestational aged-matched non-labouring controls. Although the precise role of intrauterine IL-8 at the time of parturition awaits elucidation, these data support the concept that this cytokine may be involved in the biochemical events associated with the onset and/or propagation of normal labour in the human.

Elevated plasma interleukin 6: a biochemical marker of human preterm labour.

Maternal peripheral venous plasma interleukin 6 (IL-6) concentrations were determined during human pregnancy and labour at term and preterm. During preterm labour, IL-6 concentrations were significantly elevated (p < 0.02) compared to gestationally matched, non-labouring controls (53.7 +/- 15.7 pg/ml, n = 17, and 15.4 +/- 6.4 pg/ml, n = 23, respectively). IL-6 concentrations did not vary significantly during normal pregnancy and labour at term. These data support a role for IL-6 in the pathogenesis of human preterm labour, are evidence for the contention that preterm labour is mechanistically distinct at a biochemical level from normal labour at term and identify maternal peripheral venous plasma IL-6 as a biochemical marker of this condition.