Acute and subacute effects of injury on the canine alveolar septum.

The effect of papain on the prevalence and distribution of alveolar macrophages, alveolar septal interstitial tissue gaps and epithelial cells in normal canine pulmonary alveoli was studied by light and electron microscopy. Serial sections of whole alveoli from control animals and from animals sacrificed 4 h, two weeks and one month after the instillation into one lung of crude papain in saline solution containing India ink as a marker were compared. In dogs, as in humans, there is normally a zonal distribution of alveolar macrophages and type 2 cells at alveolar junctional sites. We hypothesize that early alveolar septal injury takes place at these junctional sites, judging from concentration of alveolar macrophages and interstitial septal gaps at these sites following papain exposure, and also that septal repair activities are greatest at these sites, in view of the preponderance and high prevalence of type 2 cells occupying interstitial septal gaps in junctional zones. Consequently, the type 2 cell may play a role beyond that of merely replacing type 1 epithelial cells following alveolar septal injury.

Changes in the hypothalamic-pituitary-gonadal axis in human immunodeficiency virus-infected homosexual men.

Serum total testosterone, total 17 beta-estradiol, LH, FSH, and PRL concentrations were measured by RIA in 59 homosexual men infected with the human immunodeficiency virus (32 clinically healthy antibody-positive men (HH+), 20 men with acquired immune deficiency syndrome (AIDS), and 7 men with AIDS-related complex (ARC). The results were compared with those of 26 antibody-negative homosexual men (HH-) who served as controls. The mean serum total testosterone concentration was significantly lower in the men with AIDS [414 +/- 230 (+/- SD) ng/dL (14.5 +/- 8.0)] than in the HH- men [550 +/- 172 ng/dL (19.0 +/- 6.0 nmol/L); P less than 0.05]. The mean serum LH level was significantly higher in the men with AIDS (26 +/- 14 vs. 14 +/- 4 IU/L in HH- men; P less than 0.01) and slightly but significantly higher in the men with ARC (19 +/- 8 IU/L; 0.10 greater than P greater than 0.05). Serum FSH also was significantly higher in the men with AIDS (P less than 0.05). Serum PRL was significantly higher in the men with ARC (10 +/- 2 micrograms/L; P less than 0.05) and AIDS (16 +/- 10 micrograms/L; P less than 0.001) than in the HH- men (8 +/- 3 micrograms/L). Serum sex hormone-binding globulin levels were similar in HH- men and men with AIDS as were serum T responses to hCG administration for 2 days. These results suggest that alterations of the hypothalamic-pituitary-gonadal axis indicative of primary hypogonadism accompany human immunodeficiency virus infection in homosexual men.

Hodgkin's disease in homosexual men. An AIDS-related phenomenon?

Five cases of Hodgkin's disease in young homosexual men at risk for the acquired immune deficiency syndrome (AIDS) are reported. The mixed cellularity histologic subtype was present in each. Two also showed features of lymphocyte depletion. Four of the five patients had pathologic stage IIIB or IVB disease at presentation. In the fifth, recurrent Hodgkin's disease developed in a previously irradiated field. Three patients had opportunistic infections characteristic of AIDS. Hodgkin's disease may pursue a more fulminant course in patients at risk for AIDS and may itself be a manifestation of AIDS in this high-risk population.

Babesia rodhaini: requirement of complement for penetration of human erythrocytes.

A system has been developed in vitro in which human red cells, in the presence of fresh human (or rat) serum, are parasitized by the hemosporidian protozoan Babesia rodhaini. The ability of B. rodhaini to penetrate red cells depends on factors of the alternative complement pathway (properdin and factor B) as well as ionic magnesium and the third (C3) and the fifth (C5) components of complement. These data indicate a novel mechanism by which a parasite is able to utilize the complement system. The data are in accord with and further amplify earlier observations that demonstrated a requirement for complement in the development of babesial infection in rats.

The complement profile in babesiosis.

Rats have been infected with Babesia rodhaini, a protozoan agent that induces immune complex disease. Assays for complement have revealed depletion of C2, C3, C4, C5, and whole complement in the course of infection. No evidence of depletion in the alternative (properdin) pathway was found. These findings are consistent with the conclusion that the classical complement pathway is activated during the course of the protozoan infection.

Changes in C3 metabolism during protozoan infection (Babesia rodhaini) in rats.

Metabolism of the third component of complement (C3) and IgG was measured in rats before and during infection with the hemosporidium agent Babesia rodhaina. In the course of infection, hypocomplementemia and immune complex nephritis developed. During babesial infection, in most animals the half-life of C3 fell sharply, as did serum levels of C3; the catabolic rate for C3 sharply increased, whereas the synthetic rate sharply decreased. In contrast, the catabolic rate for IgG remained unchanged. The alteration in the metabolism of C3 in the face of nonparallel changes in IgG metabolism suggests that abnormal glomerular filtration and increased vasopermeability cannot explain the findings. Babesial infection in the rat provides a useful model for the study of acquired C3 metabolic defects that have been observed in humans with immune complex diseases.