Inflammatory Response in Preterm and Very Preterm Newborns with Sepsis

Segura-Cervantes, Enrique; Mancilla-Ramı́rez, Javier; González-Canudas, Jorge; Alba, Erika; Ballesteros, René Santillán; Morales-Barquet, Deneb Algedi; Sandoval-Plata, Gabriela; Galindo-Sevilla, Norma

doi:10.1155/2016/6740827

Cited by 32 publications

(43 citation statements)

References 29 publications

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“…2728 In addition, prematurity appears to be associated with an immune dysregulated state characterized by abnormal secretion of proinflammatory cytokines in response to different environmental stressors. 2930 The abnormal immune responses and enhanced inflammatory responses of prematurity generate a unique host environment, which, in combination with early nosocomial exposures, results in distinct microbial communities colonizing different systems. 31 32 An example is the increasingly clear link between the abnormal gut microbiota composition in PM infants and the development of necrotizing enterocolitis.…”

Section: Discussionmentioning

confidence: 99%

Nasopharyngeal Microbiome in Premature Infants and Stability during Rhinovirus Infection

Pérez

Pérez‐Losada

Isaza

et al. 2017

Journal of Investigative Medicine

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Rationale The nasopharyngeal (NP) microbiota of newborns and infants plays a key role in modulating airway inflammation and respiratory symptoms during viral infections. Premature (PM) birth modifies the early NP environment and is a major risk factor for severe viral respiratory infections. However, it is currently unknown if the NP microbiota of PM infants is altered relative to full-term (FT) individuals. Objectives To characterize the NP microbiota differences in preterm and FT infants during rhinovirus (RV) infection. Methods We determined the NP microbiota of infants 6 months to ≤2 years of age born FT (n=6) or severely PM<32 weeks gestation (n=7). We compared microbiota composition in healthy NP samples and performed a longitudinal analysis during naturally occurring RV infections to contrast the microbiota dynamics in PM versus FT infants. Results We observed significant differences in the NP bacterial community of PM versus FT. NP from PM infants had higher within-group dissimilarity (heterogeneity) relative to FT infants. Bacterial composition of NP samples from PM infants showed increased Proteobacteria and decreased in Firmicutes. There were also differences in the major taxonomic groups identified, including Streptococcus, Moraxella, and Haemophilus. Longitudinal data showed that these prematurity-related microbiota features persisted during RV infection. Conclusions PM is associated with NP microbiota changes beyond the neonatal stage. PM infants have an NP microbiota with high heterogeneity relative to FT infants. These prematurity-related microbiota features persisted during RV infection, suggesting that the NP microbiota of PM may play an important role in modulating airway inflammatory and immune responses in this vulnerable group.

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Section: Discussionmentioning

confidence: 99%

Nasopharyngeal Microbiome in Premature Infants and Stability during Rhinovirus Infection

Pérez

Pérez‐Losada

Isaza

et al. 2017

Journal of Investigative Medicine

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“…Notably, the immunity of newborns differs from that of adults in the rate of gene expression of immune system molecules via epigenetic regulation, resulting in low expression of costimulatory molecules. Newborns also lack T‐ and B‐cell memory because it relies on previous exposure events.…”

Section: Effect Of Leishmania Infection During Pregnancy On the Immunmentioning

confidence: 99%

T‐cell tolerance as a potential effect of congenital leishmaniasis on offspring immunity

Galindo-Sevilla

Mancilla-Ramı́rez

2018

Parasite Immunology

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Congenital transmission of leishmaniasis is recognized in cases detected by passive surveillance. Most cases are from low-resource countries, limiting the study of several important aspects of this route of infection, including the offspring's immune response. Studies on natural and experimentally infected animals suggest that parasites might be transmitted to the embryo or foetus at any time during pregnancy. As immune system undergoes sequential stages of development, an infection before the time of self-recognition could lead to central tolerance, making an individual specifically tolerant and susceptible to infection. In the alternative scenario, infection after self-recognition would allow the proper development of T-lymphocyte clones in response to Leishmania antigens, providing resistance to the disease. Newborns undergo a transient period of low expression of several immune surface molecules and a naïve adaptive immune response with no memory, which together might contribute to slow elimination of the parasite over several months. This insight is a proposed independent mechanism of the previously proven T-cell exhaustion and must be investigated. Analyses of infected placenta, cord blood and infant immunity are required for a better understanding of immunity in congenital leishmaniasis infection.

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“…It is generally believed that the communication among the immune, nervous and endocrine system is essential for the regulation of inflammatory response. Innate immune responses are critical for protection against lethal infection and tissue injury, but the uncontrolled production of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin-1 (IL-1), and high mobility group box-1 (HMGB1), cause the development of severe sepsis (5,6). In most septic patients, the presence of early signs also supports that the disease is resulted from an overwhelming inflammatory response to the underlying infection (7).…”

mentioning

confidence: 99%