The Evolutionary Immunology and Genomic Lab: Evolutionary impact of plague


The Brinkworth lab addresses the physiological consequences of the human experience and evolutionary past, particularly those that affect the immune system. Current projects focus on the functional divergence and diversification of primate immune systems, how past epidemics affect present day immune function diversity and how life experience affects the innate immune response. This image is the outcome of the efforts many UIUC undergrad and grad student to better understand how past plague epidemics affect current immune function in different human populations.

Our current lab members are largely from Anthropology and include: Dr. Jessica Brinkworth (Department of Anthropology), Heather Hicks (JMU, Anthropology, 2018),  Keaton McClure (UIUC MCB, 2019),  Alex Alvarado (UIUC, Anthropology, 2019),  Kyle Boshardy (UIUC, Anthropology, 2018), Priya Bhatt (UIUC, Anthropology, 2021), Tyler Hill (UIUC, Anthropology, 2018),  Sharajonnie Adam (UIUC Anthropology, 2019), Bianca Biages (University of Puerto Rico, 2021), Negin Valizadegan (UIUC Anthropology doctoral student), Celeste Kim (UIUC, Anthropology), Harsha Namburi (UIUC, MCB).

Slide preparation and photo credit: Katie Van Etten (UIUC Anthropology, 2017). Others involved in the production of this image: Keaton McClure (MCB, 2019), Priya Bhatt (Anthropology, 2021), Will Widick (Vet Med, 2019), Alex Alvarado (Anthropology, 2021), Jessica F. Brinkworth (Anthropology, PI), Luis Barreiro (University of Chicago, Co-PI) Instrument:  Zeiss LSM 700 four laser scanning confocal microscope, at Carl R. Woess Institute for Genomic Biology.


More information:

In this image chromatin is blue, red is indicative of cell death and green is Yersinia pestis (plague). These are M2 macrophages cultured from human monocytes and infected with Y. Pestis Kim5 10:1 for 24 hours. This study compares macrophage responses to Y. Pestis between human populations with assumed different historical exposure to plague.

Macrophages are  target cells for Yersinia pestis. Yersinia pestis, on infection, is an obligate intracellular pathogen. Once inside the cell, the bacteria hijacks the anti-microbial machinery of the cell, pushes the cell to transcribe an anti-inflammatory (M2) program, creates a lysosomal environment beneficial to bacterial replication and forces the cell to home to lymph node where the new bacteria will burst out of the cell and replicate unabated. That's one of traits of plague that makes it so lethal - it escapes the immune system through manipulation of macrophages, and emerges from the lymph node capable of spreading systemically. This image captures the progression towards bacteria that doesn't need a cell to replicate - the birth of the pathogen that can go wherever it pleases within the host.  

Find this work interesting? These images were created by students, as part of a research program in which many undergraduate and graduate students play a part. The Evolutionary Immunology and Genomic lab is expanding and looking for members with a passion for the work. Join us.