Requirement for In Vivo Production of IL4, But Not IL10, in the Induction of Proliferative Suppression by Filarial Parasites1 (original) (raw)
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PLoS ONE, 2011
The peritoneal cavity (PerC) is a singular compartment where many cell populations reside and interact. Despite the widely adopted experimental approach of intraperitoneal (i.p.) inoculation, little is known about the behavior of the different cell populations within the PerC. To evaluate the dynamics of peritoneal macrophage (MØ) subsets, namely small peritoneal MØ (SPM) and large peritoneal MØ (LPM), in response to infectious stimuli, C57BL/6 mice were injected i.p. with zymosan or Trypanosoma cruzi. These conditions resulted in the marked modification of the PerC myelo-monocytic compartment characterized by the disappearance of LPM and the accumulation of SPM and monocytes. In parallel, adherent cells isolated from stimulated PerC displayed reduced staining for b-galactosidase, a biomarker for senescence. Further, the adherent cells showed increased nitric oxide (NO) and higher frequency of IL-12-producing cells in response to subsequent LPS and IFN-c stimulation. Among myelo-monocytic cells, SPM rather than LPM or monocytes, appear to be the central effectors of the activated PerC; they display higher phagocytic activity and are the main source of IL-12. Thus, our data provide a first demonstration of the consequences of the dynamics between peritoneal MØ subpopulations by showing that substitution of LPM by a robust SPM and monocytes in response to infectious stimuli greatly improves PerC effector activity.
Australian Journal of Experimental Biology and Medical Science, 1986
Depressed IgG responses to ovalbumin administered with the inflammatory adjuvant, Al(OH)3, have previously been demonstrated in mice immunized 5 to 13 days after infection with Nematospiroides dubius, when the parasite is encysted in the intestinal mucosa or becoming established in the lumen. This report extends these findings to show that primary IgE and delayed-type hypersensitivity (DTH) responses, the generation of antigen-primed cells detectable in syngeneic irradiated recipients or in vitro and the recall of immunological memory are correspondingly impaired. Co-transfer experiments using irradiated recipients demonstrated weak suppressor activity in spleen cells from infected mice which was not attributable to T cells. The results suggest that N. dubius administered before immunization can impair the development of many classes of antigen-primed lymphocytes. The implications of this finding with respect to parasite survival are discussed.
International Immunology, 1996
Despite this immune suppression, responses indicative of T h 2 subset activation are present, including unusually high levels of specific lgG4. We tested the possibility that infection with filarial nematodes causes a reduction in the co-stimulatory or antigen-presenting capacity of macrophages resulting in a failure to activate specific T cells. Adherent peritoneal exudate cells (PEC) from mice implanted with adult B. malayi were used to present antigen to the conalbumin-specific T cell clone, D10.G4. Proliferation of the D10 cells at even background levels was completely blocked by the presence of implant-derived adherent PEC. However, cytokine production by these cells in response to antigen was intact, and thus PEC from implanted mice are capable of functionally processing and presenting antigen. The elicitation of a suppressive cell population was specific for live adults as cells from mice implanted with dead adult parasites effectively stimulated D10 proliferation. The block in cellular proliferation is not due to the production of factors typically associated with macrophage suppression such as nitric oxide, prostaglandins or catalase. These observations are consistent with the T cell hyporesponsiveness seen in human cases of patent Brugia infection and may provide a murine model for the immune suppression seen in lymphatic filariasis.
1994
Among other effects, prostaglandins (PG) of the E series are known to inhibit several acute and chronic inflammatory conditions in vivo and proinflammatory cytokine production by activated macrophages in culture. The research presented here demonstrates that the inhibitory effect of PGE2 on tumor necrosis factor oe (TNF-oL) and interleukin 6 (IL-6) production by lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages involves IL-10. In a dose-dependent manner, PGE2 inhibits LPS-induced release of TNF-ol and IL-6, but not of lactate or nitric oxide. The decrease in the level of these cytokines is inversely proportional to the increase in immunoreactive IL-10. This differential inhibitory effect of PGE2 is mimicked by agents that elevate intracellular levels of cAMP, but not cGMP. Neutralizing anti IL-10 antibody but not neutralizing antibodies against other macrophage secretory products (IL-6, leukemia inhibitory factor, and transforming growth factor fl [TGF-fl]), signific...