Interleukin-6 production by human monocytes stimulated with Cryptococcus neoformans components

Abstract

In order to ascertain if Cryptococcus neoformans components can induce interleukin-6 (IL-6) production, we stimulated human whole blood with purified capsular products. Their potencies in stimulating IL-6 release were mannoproteins > galactoxylomannan ‫؍‬ glucuronoxylomannan > ␣(1-3)glucan. IL-6 production was tumor necrosis factor alpha independent and required the presence of monocytes and plasma. Since IL-6 can stimulate replication of the human immunodeficiency virus in monocytic cells, these findings may be clinically relevant.

“Inflamm‐aging” influences immune cell survival factors in human bone marrow

“…Antigen‐presenting CD11c hi and CD14 + cells have been considered to be the main cell types producing APRIL and IL‐6 and producing and trans‐presenting IL‐15 to T cells in the BM . CD34 + myeloid progenitor cells have also been found to produce IL‐15 .…”

“…Studies in mice suggest that long‐lived plasma cells reside in survival niches organized by reticular stromal cells expressing the chemokine CXCL‐12 (stromal cell‐derived factor 1; SDF1) . Survival factors such as a proliferation‐inducing ligand (APRIL) and IL‐6, mainly produced by myeloid cell types, are also known to be important for the maintenance of long‐lived plasma cells . Effector/memory CD4 + T cells have been described also to migrate to BM niches where they interact with VCAM‐1 + stromal cells producing the survival factor IL‐7 .…”

Alzheimer′s Disease: APP, Gamma Secretase, APOE, CLU, CR1, PICALM, ABCA7, BIN1, CD2AP, CD33, EPHA1, and MS4A2, and Their Relationships with Herpes Simplex, C. Pneumoniae, Other Suspect Pathogens, and the Immune System

“…IL6 plasma and CSF levels have been reported to be increased in Alzheimer's disease and the secretion of IL6 from monocytes is increased [287][288][289]. IL6 plasma levels are raised by infection with C. pneumoniae [290] or Helicobacter pylori [291], and IL6 production in monocytes is stimulated by C. neoformans [292]. Stressactivated corticosterone is also able to reactivate the virus [293] (pathway = steroid hormone biosynthesis: COMT, CYP19A1, HSD11B1).…”

Cryptococcus neoformans and its cell wall components induce similar cytokine profiles in human peripheral blood mononuclear cells despite differences in structure

“…Healthy people are capable of mounting an ad-equate (cellular) protective immune response against cryptococci. Furthermore, animal models and in vitro studies have shown that the presence of cytokines such as TNF-K, IFN-Q, IL-1L and IL-6 contributes to a host defense against C. neoformans [12]. TNF-K has been described to enhance antifungal activities of polymorphonuclear leukocytes and mononuclear phagocytes against Aspergillus fumigatus, a comparable clinically important fungus [25].…”

“…Recently, we demonstrated the presence of low levels of TNF-K and IL-10, IFN-Q was seen in only a minority of the patients, high levels of IL-1L, IL-6 and IL-8 were present in the cerebrospinal £uid (CSF) of cryptococcosis patients [10]. Several other investigators reported on the in vitro induction of cytokines in effector cells after stimulation with C. neoformans or its components [11,12]. However, levels of cytokine induction vary strongly, depending on the exact experimental conditions [13].…”