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Zaki, H.

Publications and source records attributed to Zaki, H..

2 recordsLinked to original sources

Larval zebrafish exhibit collective motion behaviors in constrained spaces

Collective behavior may be elicited or can spontaneously emerge by a combination of interactions with the physical environment and conspecifics moving within that environment. To investigate the relative contributions of these factors in a small millimeter-scale swimming organism, we observed larval zebrafish, interacting at varying densities under circular confinement. Our aim was to understand the biological and physical mechanisms acting on these larvae as they swim together inside circular confinements. If left undisturbed, larval zebrafish swim intermittently in a burst and coast manner and are socially independent at this developmental stage, before shoaling behavioral onset. We report here our analysis of a new observation for this well-studied species: in circular confinement and at sufficiently high densities, the larvae collectively circle rapidly alongside the boundary. This is a new physical example of self-organization of mesoscale living active matter driven by boundaries and environment geometry. We believe this is a step forward toward using a prominent biological model system in a new interdisciplinary context to advance knowledge of the physics of social interactions.

animal behavior and cognition

SARS-CoV-2 spike protein induces inflammation via TLR2-dependent activation of the NF-κB pathway

Pathogenesis of COVID-19 is associated with a hyperinflammatory response; however, the precise mechanism of SARS-CoV-2-induced inflammation is poorly understood. Here we investigated direct inflammatory functions of major structural proteins of SARS-CoV-2. We observed that spike (S) protein potently induces inflammatory cytokines and chemokines including IL-6, IL-1{beta}, TNFa, CXCL1, CXCL2, and CCL2, but not IFNs in human and mouse macrophages. No such inflammatory response was observed in response to membrane (M), envelope (E), and neucleocapsid (N) proteins. When stimulated with extracellular S protein, human lung epithelial cells A549 also produce inflammatory cytokines and chemokines. Interestingly, epithelial cells expressing S protein intracellularly are non-inflammatory, but elicit an inflammatory response in macrophages when co-cultured. Biochemical studies revealed that S protein triggers inflammation via activation of the NF-{kappa}B pathway in a MyD88-dependent manner. Further, such an activation of the NF-{kappa}B pathway is abrogated in Tlr2-deficient macrophages. Consistently, administration of S protein induces IL-6, TNF-a, and IL-1 {beta} in wild-type, but not Tlr2-deficient mice. Together these data reveal a mechanism for the cytokine storm during SARS-CoV-2 infection and suggest that TLR2 could be a potential therapeutic target for COVID-19.

immunology