DOI: 10.5061/dryad.sf7m0cgkz
title: Data from: Aryl hydrocarbon receptor activation alters emergency hematopoiesis during influenza A virus infection

description: Hematopoietic stem and progenitor cells (HSPCs) produce all cells of the
 blood and immune system in a process known as hematopoiesis. During
 infection, there is an increased demand for immune cells, which causes
 HSPCs to rapidly and transiently modify cellular output, a response
 described as emergency hematopoiesis. Small molecules from the host
 environment may contribute to signals that regulate emergency
 hematopoiesis, providing a means to influence important processes during
 infection. Environmental exposures have long been associated with altered
 immune responses in the human population and experimental studies.
 Specifically, chemicals that bind the aryl hydrocarbon receptor (AHR)
 modulate immune responses in a broad range of contexts, including during
 viral infection. Separate studies have shown that AHR signaling also
 influences steady-state hematopoiesis. Using two different AHR ligands,
 2,3,7,8- tetrachlorodibenzo-p-dioxin (TCDD) and
 2-(1H-indol-3-ylcarbonyl)-4-thiazole-carboxylic acid methyl ester (ITE),
 we characterized the impact of AHR activation on the proportion of HSPC
 and lineage-committed progenitor cells over the course of an influenza A
 virus infection in mice. AHR activation via these two ligands had a
 distinct impact on HSPCs, yet affected monocytes in the blood and lung
 similarly. For example, AHR activation with TCDD, but not ITE, increased
 myeloid-biasing among HSPC. However, the frequency of monocytes in the
 lung was reduced by either TCDD or ITE treatment. Using Vav1CreAhrfxfx
 mice, we showed that these effects depend on AHR expression in
 hematopoietic cells. Collectively, these findings highlight the
 differential effects of AHR ligands and their role in regulating emergency
 hematopoiesis in response to a common respiratory pathogen.
description: # Data from: Aryl hydrocarbon receptor activation alters emergency
 hematopoiesis during influenza A virus infection Dataset DOI:
 [10.5061/dryad.sf7m0cgkz](https://doi.org/10.5061/dryad.sf7m0cgkz) ##
 Description of the data and file structure Enclosed are tables of the
 percentage and number of hematopoietic stem and progenitor cells in the
 bone marrow of mice, the average percentage and number of platelets, red
 blood, and monocytes in the blood of mice, and the mean percentage and
 number of monocytes in the lungs of mice. ### Files and variables ####
 File: Data.xlsx **Description:** Mean percentage and number of
 hematopoietic stem and progenitor cells in the bone marrow and cells of
 the blood in mice ##### Variables * Mice were treated with vehicle-control
 (peanut oil), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD),
 or 2-(1H-indol-3-ylcarbonyl)-4-thiazole-carboxylic acid methyl ester
 (ITE)*.* The following day, mice were infected with the influenza virus
 (HKx31, 120HAU). Mice were sacrificed on multiple days after infection,
 and bone marrow, blood, and lungs were collected. Single-cell suspensions
 of bone marrow and lung were obtained, and cells were stained for flow
 cytometry. Blood was analyzed bya complete blood count (CBC) analyzer for
 platelets and red blood cells. Blood was also stained for flow cytometry
 to identify monocytes. Experiments consisted of 4-9 mice per treatment
 group per day of infection. * Data is represented as the mean percentage
 or number of cells from 4-9 mice per treatment group per day of
 infection.  * Hematopoietic stem and progenitor cells, monocytes in the
 blood and lung, are derived from flow cytometry data * Platelet and red
 blood cell numbers were derived from a complete blood count (CBC)
 analyzer. * Across infection, BM cellularity rises early (peaks ~day 5)
 and then declines by days 7–12 in both groups, with TCDD generally showing
 lower or delayed recovery compared to Vehicle. HSPCs expand markedly after
 infection, peaking around day 7, with TCDD often exaggerating HSPC numbers
 despite similar or modestly altered percentages. Lineage bias shifts
 dynamically: early myeloid (MPPGM/MPPM) expansion dominates, while
 lymphoid (MPPLy) fractions drop at day 5 and rebound strongly by day 7.
 Overall, TCDD alters the magnitude and timing of hematopoietic responses
 to infection rather than completely changing lineage trajectories. ###
 Software Any program that will open a spreadsheet, such as Excel, is
 recommended. #### Supplemental Information File:
 Supplemental_Information.docx **Description:** Supplementary figures and
 data tables ##### Variables * All data is represented as the mean and
 standard error  * All statistical testing used in each figure and table is
 noted in the Figure/Table legend