Lung Antimicrobial Defenses in the Newborn

Wilson, Christopher

doi:10.1055/s-2007-1011491

Cited by 9 publications

(4 citation statements)

References 46 publications

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“…The results of this study demonstrating the presence of intact and viable GBS within macrophages are not at odds with the in vivo observation that macrophages from lungs of infants who succumbed to GBS infection contain disrupted GBS 59 . On the contrary, under our in vitro experimental conditions, the absence of an important macrophage‐activating factor, such as IFN‐γ and of its complex co‐operative interactions with other cytokines, would not favour an effective macrophage activation.…”

Section: Discussioncontrasting

confidence: 59%

Group B streptococci persist inside macrophages

et al. 1998

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SUMMARYGroup B streptococci (GBS ) are an important cause of neonatal sepsis, pneumonia and meningitis. In the early phase of infection, macrophages and polymorphonuclear cells (PMN ) are the first immune cells that interact with GBS. In this in vitro study, to gain insight into GBS-macrophage interaction in the absence of type-specific antibodies, we examined the features of GBS survival in thioglycollate-elicited murine peritoneal macrophages and the effect of GBS on the protein kinase C (PKC )-dependent transduction pathway. Our results demonstrate that type Ia GBS, strain 090 (GBS-Ia) and type III GBS strain COH 31r/s (GBS-III ), after in vitro phagocytosis survive and persist intracellularly in macrophages for up to 24 and 48 hr, respectively. However, macrophage activation by interferon-c (IFN-c) and lipopolysaccharide from Escherichia coli (LPS ) caused a significant reduction in the time of intracellular persistence. Macrophage activation by IFN-c and LPS seems to be a multifactorial event involving multiple intracellular signal pathways also including PKC. Since PKC is one of the components in the signal network leading to macrophage activation and an important target for several intracellular micro-organisms, we wondered whether PKC could have a role in intracellular GBS survival. Both PKC depletion by treatment with phorbol 12-myristate 13-acetate (PMA) for 18 hr and PKC inhibition by Calphostin C rendered macrophages more permissive for the intracellular GBS survival. Furthermore, GBSinfected macrophages were unable to respond to PMA and LPS, activators of PKC, by inducing antimicrobial activity. The ability of GBS to impair PKC-dependent cell signalling was also demonstrated by the reduced c-fos gene expression in GBS-infected macrophages with respect to control macrophages, after LPS stimulation. In conclusion, our results indicate that GBS survive in macrophages and impairment of PKC signal transduction contributes to their intracellular survival. INTRODUCTIONcorrelates with the susceptibility or resistance of neonates to GBS infection.15,16 Group B streptococci (GBS ) are the major cause of pneuThe discovery that macrophages can phagocytose GBS in monia, sepsis and meningitis in neonates and a serious cause the absence of immune serum by C3-dependent binding17 and of mortality or morbidity in immunocompromised adults.1,2 C3-independent binding using complement receptor type three The main virulence factor of GBS is thought to be the capsular (CR3)18 suggests that there is also a potential role for antibodypolysaccharide because of its antiphagocytic properties.3,4 In independent mechanisms in resistance to GBS infection. resistance to GBS infection, a central role is played by antiHowever, the recent demonstration that type III GBS phagobodies to the type-specific capsular polysaccharide and complecytosed by a macrophage-like line J774 in the absence of typement which potentiate in vitro phagocytosis and GBS killing specific antibodies survived within its host cell,19 seems to by phagocytic cells...

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Section: Discussioncontrasting

confidence: 59%

Group B streptococci persist inside macrophages

et al. 1998

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“…2,35,36 Infants born at an early and immature gestational age have additional risks for lung injury because of severe lung immaturity and an impaired immune system, insufficient surfactant content, and decreased levels of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) compared to term infants. [37][38][39] Furthermore, important structural changes in the developing lung (i.e., appearance of the capillary network, histologically distinguishable alveoli, marked increase in the gas exchange surface area, and development of type II pneumocytes) occur from 28 weeks through 40 weeks of postconceptional age. 40 Extrauterine existence during this period is dangerous for premature infants.…”

Section: Neonatal Lung Inflammationmentioning

confidence: 99%

Markers and mediators of inflammation in neonatal lung disease

1997

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“…Os linfócitos estão em número normal no RN e têm função adequada em situações normais. A mobilidade, assim como a adesividade, é menor quando se trata de linfócito T. Há poucos dados quanto à fagocitose, que parece estar diminuída 7 . Os linfócitos B apresentam na superfície IgG ou IgA comparável no adulto, mas o defeito está na função.…”

Section: Introductionunclassified

Concentrações séricas de imunoglobulinas em sangue do funículo umbilical e em sangue materno no momento do parto

Hironaka

Casanova

2003

Acta Cir. Bras.

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OBJETIVO: Identificar as concentrações das imunoglobulinas no sangue do funículo umbilical comparando-as às do sangue materno no momento do parto. MÉTODOS: Foram analisadas amostras colhidas de 323 RN e de 321 mães pelo método de turbidimetria. Os resultados foram submetidos à análise estatística, estabelecendo-se coeficiente de correlação r e nível de significância p 0,05. As retas de regressão obedeceram ao limite de 95%. RESULTADOS: Houve aumento progressivo de IgG sérica do RN, diretamente proporcional à idade gestacional ( r=0,31;p=0,0001); quanto ao peso de nascimento, esta relação não foi tão evidente (r=0,14;p=0,008), possivelmente por estarem incluídos na amostra RNPT e RN com restrição ao crescimento intra-uterino. O aumento da IgG do RN foi maior que o da mãe (r=0,20;p=0,0001). Houve queda de concentração da IgM com o aumento da idade materna e aumento da IgM e IgA maternas comparadas à IgG do RN. Observou-se queda da concentração de IgG do funículo umbilical quando relacionada ao tempo maior de ruptura da bolsa (r=-0,13;p=0,018). CONCLUSÕES: A concentração de IgG no funículo umbilical aumentou proporcionalmente à idade gestacional e diminuiu com tempo maior de ruptura de membranas.Concentrações de IgM e IgA no sangue materno aumentaram significativamente quantdo comparadas à IgG do funículo umbilical e a IgM diminuiu significativamente com o aumento da idade materna.

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Lung Antimicrobial Defenses in the Newborn

Cited by 9 publications

References 46 publications

Group B streptococci persist inside macrophages

Group B streptococci persist inside macrophages

Markers and mediators of inflammation in neonatal lung disease

Concentrações séricas de imunoglobulinas em sangue do funículo umbilical e em sangue materno no momento do parto

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