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Michael Serralha

Michael Serralha is a Research Assistant in the Chronobiology and ORIGINS teams at The Kids Research Institute Australia.

Innate immune activation occurs in acute food protein–induced enterocolitis syndrome reactions

Food reactions in food protein–induced enterocolitis syndrome are predominantly underpinned by activation of the innate immune system

Upper Airway Cell Transcriptomics Identify a Major New Immunological Phenotype with Strong Clinical Correlates in Young Children with Acute Wheezing

Asthma exacerbations in children can be divided into IRF7hi versus IRF7lo phenotypes with associated differences in clinical phenotypes

Persistent activation of interlinked type 2 airway epithelial gene networks in sputum-derived cells from aeroallergen-sensitized symptomatic asthmatics

Our findings provide new insight into the molecular mechanisms operative at baseline in the airway mucosa in atopic asthmatic with natural aeroallergen exposure

Protection against maternal infection-associated fetal growth restriction: Proof-of-concept with a microbial-derived immunomodulator

This study suggests that broad-spectrum protection-of-pregnancy against infection-associated inflammatory stress represents an achievable therapeutic goal

Respiratory viral infections and host responses; insights from genomics

Review of the viral sensing pathways and organizing principles that govern the innate immune response to infection

Rapid recruitment of CD14+ monocytes in experimentally induced allergic rhinitis in human subjects

Mononuclear phagocyte population is directly involved in the production of proinflammatory chemokines that attract other immune cells

Rhinovirus-induced asthma exacerbations and risk populations

Asthma exacerbations are heterogeneous conditions that involve the complex interplay between environmental exposures and innate and adaptive immune function

The effects of in utero vitamin D deficiency on airway smooth muscle mass and lung function

In this study, we aimed to uncover the molecular mechanisms contributing to altered lung structure and function.