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Cytokine Response to Group B Streptococcus Infection in Mice
Author(s) -
Emanuela Rosati,
Katia Fettucciari,
Lucia Scaringi,
Paola Cornacchione,
Sabatini,
Letizia Mezzasoma,
Laura Lucia Rossi,
Pierfrancesco Marconi
Publication year - 1998
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1998.00305.x
Subject(s) - cytokine , spleen , biology , immunology , in vivo , tumor necrosis factor alpha , western blot , intraperitoneal injection , northern blot , in vitro , interleukin 10 , microbiology and biotechnology , streptococcus , messenger rna , bacteria , gene , endocrinology , genetics , biochemistry
This study was undertaken to better understand the complex relationship between specific and non‐specific host defence mechanisms and group B streptococci (GBS). A comprehensive kinetics analysis of cytokine mRNA expression was performed, by Northern blot assay, in peritoneal exudate cells (PEC) and spleen cells (SC) recovered from CD‐1 mice at various times during the course of an intraperitoneal infection with a lethal dose (5 × 10 3 microorganisms/mouse) of type Ia GBS, reference strain 090 (GBS‐Ia). Analysis of cytokines involved in the development of a specific T H response shows that GBS‐Ia in PEC induce only a weak increase of IL‐2 mRNA expression and in SC a cytokine pattern characterized by IL‐2, IFN‐γ and IL‐12 in the absence of IL‐4, IL‐5 and IL‐10. This selected cytokine pattern could provide appropriate conditions for the development of a T H 1 response. Analysis of inflammatory cytokines, which are usually induced early during an in vivo infection, shows that there is a significant expression of mRNA specific for IL‐1β, TNFα and IL‐6, both in PEC and SC only at 24 h which persists at a high level until 36 h. This delayed cytokine induction, accompanied by the contemporary activation of splenic phagocytic cells, occurs only when the number of GBS‐Ia is extremely high. In fact, at 24 h GBS‐Ia have heavily colonized all organs. In vitro infection of thioglycollate‐elicited peritoneal macrophages confirms that the ability of GBS‐Ia to induce a strong inflammatory cytokine response depends strictly on the number of infecting microorganisms. Indeed, macrophages respond to GBS‐Ia with a very rapid induction of IL‐1β and TNFα mRNA when infected at a ratio of 1:10, but not at 100:1. Two major observations emerged from this study: (1) GBS‐Ia, by inducing a cytokine pattern which seems to favour development of a T H 1 response, could evade antibody production essential for resistance to GBS; and (2) inflammatory cytokine response is induced when a heavy microbial invasion of the host has already occurred. These novel features of GBS‐Ia could contribute to the development and progression of lethal infection in mice.