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

被引:24
作者
Korir, Michelle L. [1 ]
Manning, Shannon D. [1 ]
Davies, H. Dele [2 ]
机构
[1] Michigan State Univ, Dept Microbiol & Mol Genet, E Lansing, MI 48824 USA
[2] Univ Nebraska Med Ctr, Coll Med, Dept Pediat, Omaha, NE 68198 USA
关键词
group B streptococcus; immunology; inflammation; prevention; VIRULENCE GENE-EXPRESSION; LATE-ONSET; CAPSULAR POLYSACCHARIDE; INTRACELLULAR SURVIVAL; COMPLEMENT-SYSTEM; SEROTYPE-III; CORD-BLOOD; COLONIZING STRAINS; NONPREGNANT ADULTS; BACTERIAL PATHOGEN;
D O I
10.1128/CMR.00019-17
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Although a normal member of the gastrointestinal and vaginal microbiota, group B Streptococcus (GBS) can also occasionally be the cause of highly invasive neonatal disease and is an emerging pathogen in both elderly and immuno-compromised adults. Neonatal GBS infections are typically transmitted from mother to baby either in utero or during passage through the birth canal and can lead to pneumonia, sepsis, and meningitis within the first few months of life. Compared to the adult immune system, the neonatal immune system has a number of deficiencies, making neonates more susceptible to infection. Recognition of GBS by the host immune system triggers an inflammatory response to clear the pathogen. However, GBS has developed several mechanisms to evade the host immune response. A comprehensive understanding of this interplay between GBS and the host immune system will aid in the development of new preventative measures and therapeutics.
引用
收藏
页码:973 / 989
页数:17
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