Different Sequence Strains ofStreptococcus agalactiaeElicit Various Levels of Cytokine Production

Abstract

Group B streptococcus (GBS) is the most common cause of neonatal and obstetric sepsis and an increasingly important cause of septicemia in elderly subjects and immunocompromised patients. Our aim was to evaluate whether different genotypes of GBS may induce a different production of pro-inflammatory and anti-inflammatory cytokines. We used multilocus sequence typing to identify 71 clones isolated from asymptomatic healthy carriers and symptomatic individuals. All these clinical isolates were used to infect purified human monocytes. TNF-alpha, IL-6, IL-8 and IL-10 secretion was measured. Fifteen allelic sequence types (STs) were identified. The MLST (multilocus sequence typing) analysis grouped the bacteria into four different lineages (clonal cluster) and two of these were closely involved in the infection of symptomatic subjects: CC17 and CC19. Furthermore, CC17 and CC19 stimulated TNF-alpha, IL-6 and IL-8 production significantly more than the other lineages, while CC17 induced a decreased IL-10 production. These results suggest the existence of differences in immune response to infection with particular genotypes of GBS.

Maternal self-reported genital tract infections during pregnancy and the risk of selected birth defects

“…These infections induce immune responses in the host and lead to changes in the concentrations of inflammatory mediators such as cytokines (Vats et al, 2007; De Francesco et al, 2008). Common variants in the gene encoding tumor necrosis factor, a cytokine, have been examined for an association with limb deficiency; being heterozygous for the −376G>A variant was associated with a twofold increased odds for limb deficiency compared to GG homozygotes, but this was not statistically significant (Carmichael et al, 2006).…”

Group B Streptococcal Maternal Colonization and Neonatal Disease: Molecular Mechanisms and Preventative Approaches

“…Group B Streptococcus cytokine stimulation has been examined in many human immune, epithelial, and endothelial cells that comprise host barriers and defenses including dendritic cells ( 140 ), monocytes ( 141 ), lung epithelial cells ( 142 ), urinary bladder epithelial cells ( 143 ), vaginal and cervical epithelial cells ( 63 ), brain microvascular endothelial cells ( 144 ), astrocytes ( 145 ), and coronary artery endothelial cells ( 146 ). Intravenous or intraperitoneal GBS infection in mouse models induced robust production of TNF-α, IL-1β, and IL-6 ( 147 , 148 ); and these cytokines as well as IFN-γ, IL-8, and IL-10 were activated upon intraperitoneal challenge of humanized mice ( 149 ).…”

Intrinsic Maturational Neonatal Immune Deficiencies and Susceptibility to Group B Streptococcus Infection

“…GBS strains belonging to different sequence types also elicited different cytokine responses in primary human monocyte cells. More specifically, infection by strains belonging to CC17 and -19, both of which are more frequently associated with infection (10), resulted in significantly higher levels of production of TNF-␣, IL-6, and IL-8 than those induced by strains of other lineages (70).…”