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In mammals, multiple recognition systems have co-evolved to preserve the normal interactions with the commensal flora and to initiate immune responses to invading pathogens and perturbations in tissue homeostasis. Toll-like receptors predominantly recognize pathogen-associated molecular patterns (PAMPs) found in microbes that are present in the extracellular or endosomal compartments. Meanwhile, a multitude of intracellular (cytosolic) receptors recognize intracellular PAMPs and host-derived signals, also known as damage-associated molecular patterns (DAMPs). The cooperation between these compartmentalized surveillance systems allows organisms to sense and respond to a large number of infectious and sterile insults to the host.


In particular, we are interested in the intracellular sensing platforms known as the inflammasomes. Inflammasomes are multi-protein complexes assembled around a set of core components that include a sensor protein, an adaptor protein (apoptosis-associated speck-like protein containing a CARD (ASC)), and an inflammatory caspase. Sensor proteins belong to two families of proteins: the NLR family and the PYHIN family. The core function of inflammasomes is the cleavage of the precursors of the cytokines IL-1β and IL-18 into their bioactive forms, and in the initiation of a form of cell death called pyroptosis.


We have identified inflammasomes as critical regulators of the intestinal microflora composition and therefore essential to prevent the aberrant expansion of bacterial species which are normally suppressed. Expansion of these bacterial communities has significant deleterious consequences at the local (intestinal inflammation) and systemic (severe metabolic abnormalities) levels.


We are interested in understanding the initiating events that lead to constitutive activation of inflammasomes and the effector mechanisms that prevent dysbiosis and obesity-associated disorders.

© 2020 by HENAO-MEJÍA LAB. 

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