Zoe Matacchiera - Graduate Student

Influenza A virus (IAV) is a major cause of respiratory infections in both humans and animals worldwide. The host immune system relies on both innate and adaptive responses to combat the virus. A crucial component of the innate immune response is the ability of tissue-resident macrophages (TRMs) to sense pathogens and infection-induced tissue damage. TRMs are found in nearly all tissues and are defined by their embryonic origin and self-renewal capacity, making them largely independent of bone marrow progenitors.  In the lungs, two distinct populations of TRMs—alveolar and interstitial macrophages—are classified based on their location, function, and cell-surface markers. However, the dynamics of these cells during IAV infection remain poorly understood. Our lab recently demonstrated that intracellular pathogens that elicit IFN-γ signaling trigger the depletion of multiple TRM populations, resulting in their replacement by monocyte-derived macrophages, which are generally better equipped to control microbial and viral infections.

Using multi-parameter flow cytometric analysis, we are investigating this phenomenon in alveolar and interstitial lung macrophages and assessing their roles in immune defense against IAV. Our findings indicate that influenza infection causes a marked depletion of embryonically seeded alveolar macrophages, followed by their replacement with interstitial macrophages rather than monocyte-derived cells. Additional experiments suggest that this transition is driven, in part, by infection-induced changes in the availability of essential growth factors required to sustain different populations of TRMs.

The primary aims of this project are to define the molecular mechanisms underlying metabolic shifts in lung macrophages and to elucidate their roles in host defense against viral pathogens such as influenza.

 Dec 11, 2025 @ 12:00 p.m.
 Medical Center | K307 (3-6408)