Production and properties of histamine-releasing factor of guinea pigs

The production of histamine-releasing factor (HRF) by human mononuclear cells has previously been reported. In this paper we describe the production of HRF by guinea pig spleen cells, thymocytes, and PBMC. Guinea pig lymphoid cells were cultured either alone or in the presence of mitogens (PHA and Con A) or specific Ag(OVA and keyhole limpet hemocyanin) and the dialyzed cell-free supernatant was tested for histamine-releasing activity on guinea pig lung mast cells and blood basophils. Lung mast cells were isolated by enzymatic digestion and partially purified by countercurrent elutriation and discontinuous Percoll gradient centrifugation. Guinea pig spleen cells, thymocytes, and PBMC spontaneously produced significant amounts of HRF. The production was enhanced upon stimulation with PHA or specific Ag in animals immunized with Ag in CFA. Two distinct species of HRF were identified with m.w. of 50,000 to 70,000 and 5000 to 8000 by gel chromatography. HRF is a trypsin- and chymotrypsin-sensitive heat-stable protein. It does not bind to Con A-Sepharose and its production is not inhibited by tunicamycin. HRF-induced histamine release from lung mast cells is a temperature-dependent process and is complete in 10 min at 37 degrees C. Intradermal injection of HRF caused an immediate ear-swelling reaction in guinea pigs. The most severe ear-swelling reactions did not resolve within 1 h, but instead evolved over a period of 12 to 24 h.     

Complement-requiring neutralizing antibody in guinea pigs with primary and recurrent genital herpes

Guinea pigs inoculated intravaginally with herpes simplex virus type 2 (HSV-2) strain 1868 produced a serum complement-requiring neutralizing (CRN) antibody during primary acute infection, i.e., 10 days postinoculation. The CRN antibody titers in the guinea pig sera decreased to less than 1:10 after heating at 56 degrees C for 30 min. It was found that 32 units of complement were necessary to obtain a satisfactory HSV-2 neutralizing antibody titer. Nonheated sera significantly reduced virus infectivity titers when mixed with 3.5 log10 PFU of HSV-2 and incubated at 37 degrees C for 20 to 60 min (P less than 0.001), whereas the same sera after heating at 56 degrees C for 30 min showed no inhibitory effect. Only 27.3% of infected guinea pigs had low serum non-CRN antibody titers ranging from 1:20 to 1:40. In addition, no evidence of increase in CRN antibody titers was noted during spontaneous recurrent genital herpes infection.     

Suppression of antibody synthesis to dinitrophenylated bovine gamma globulin in contact-sensitized guinea pigs.

The anti-DNP response to DNP-BGG is substantially suppressed in guinea pigs sensitized to DNCB. The degree of antibody suppression varies with the mode of skin sensitization and with the degree of conjugation of the challenging immunogen. Suppression of the anti-HSA response was also induced by the prior injection of CFA.     

Interstitial pneumonia in guinea pigs

Interstitial pneumonia was observed in 12 male guinea pigs. Grossly, the lung showed clear white areas in the parenchyma. Histological changes in the lung consisted of interstitial pneumonia and formation of granulomas accompanied by bacterial clumps. It was thought that this disorder might have occurred as a bacterial infection.     

Induction of delayed hypersensitivity in guinea pigs by staphylococcal cell wall components

The subcutaneous injection of 100 micrograms of staphylococcal cell-wall peptidoglycan in Freund's incomplete adjuvant leads to the development of sensitization which can be detected on days 7-35 by the splenocyte migration inhibition test. Sensitization can be detected with peptidoglycan, as well as with staphylococcal cell walls. Teichoic acids produce no such effect. The sensitization of guinea pigs with whole staphylococcal cells introduced in three injections also leads to the development of delayed hypersensitivity specific to staphylococcal cell walls, peptidoglycan, but not teichoic acids.     

Experimental cryptococcosis in guinea pigs

A guinea pig model was used to evaluate immune response to Cryptococcus neoformans. This model shared characteristics with cryptococcosis in humans. Twenty five guinea pigs injected intraperitoneally with 10(7) viable C. neoformans cells developed disseminated disease. Forty days after infection all guinea pigs were killed and autopsy performed. C. neoformans growth in the lungs, brains, livers and spleen of the infected animals were determined. Furthermore, the immune response was characterized by moderate degree of delayed-type hypersensitivity and humoral response. In some organs was observed neutrophil and lymphocyte infiltration with presence of cryptococci cells. The infiltration observed in the organs was probably a consequence of an immune reaction.