C. L. Larson

National Institute of Allergy and Infectious Diseases

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Robert A. Heinzen

National Institute of Allergy and Infectious Diseases

Mary Baker

Texas Tech University

Paul A. Beare

National Institute of Allergy and Infectious Diseases

Robert E. Baker

George Mason University

E. Ribi

Twin Cities Orthopedics

Michael E. Konkel

Washington State University

R. N. Ushijima

Battelle

Lloyd L. Smrkovski

Armed Forces Institute of Pathology

Diane C. Cockrell

National Institutes of Health

W. C. Wicht

National Institutes of Health

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National Institutes of Health

National Institute of Allergy and Infectious Diseases

Washington State University

University of Montana

United States Public Health Service

National Center for Advancing Translational Sciences

University of Illinois Urbana-Champaign

Rocky Mountain Research (United States)

Virginia Commonwealth University Medical Center

Virginia Commonwealth University

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An Epidemic of a Severe Pneumonitis in the Bayou Region of Louisiana: IV. A Preliminary Note on Etiology

Public Health Reports (1896-1970) (1944)

B. J. Olson C. L. Larson

Etiology

Pneumonitis

10.2307/4585063

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Citations (17)

Plaque-forming cells in the spleens of rabbits immunized with viable BCG bacilli or oil cell wall vaccine from Mycobacterium bovis.

PubMed (1968)

C. L. Larson Mary Baker Daniel T. Smith

BCG vaccine

10.1164/arrd.1968.97.4.715

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Citations (3)

Comparison of antigenic fractions obtained by Seibert and Affronti method from protoplasm and culture filtrates of Mycobacterium bovis (BCG).

PubMed (1970)

C. L. Larson Robert E. Baker Mary Baker

Protoplasm

10.1164/arrd.1970.101.6.979

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Citations (0)

A TEN-YEAR POPULATION STUDY OF THE RABBIT TICK HAEMAPHYSALIS LEPORIS–PALUSTRIS1

American Journal of Epidemiology (1943)

R. G. Green Carla A. Evans C. L. Larson

Journal Article A TEN-YEAR POPULATION STUDY OF THE RABBIT TICK HAEMAPHYSALIS LEPORIS–PALUSTRIS Get access R. G. GREEN, R. G. GREEN 2Department of Bacteriology and Immunology, University of MinnesotaMinneapolis, Minn. Search for other works by this author on: Oxford Academic PubMed Google Scholar C. A. EVANS, C. A. EVANS 3Division of Game and Fish, Minnesota Department of Conservation, St. Paul, Minn.Department of Bacteriology and Immunology University of MinnesotaMinneapolis, Minn. Search for other works by this author on: Oxford Academic PubMed Google Scholar C. L. LARSON C. L. LARSON 4Fish and Wildlife Service, U. S. Department of the Interior. More recently with the U. S. Public Health ServiceWashington, D. C. Search for other works by this author on: Oxford Academic PubMed Google Scholar American Journal of Epidemiology, Volume 38, Issue 3, November 1943, Pages 260–281, https://doi.org/10.1093/oxfordjournals.aje.a118888 Published: 01 November 1943 Article history Received: 08 May 1943 Published: 01 November 1943

10.1093/oxfordjournals.aje.a118888

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Citations (16)

A DESCRIPTION OF SHOCK DISEASE IN THE SNOWSHOE HARE1

American Journal of Epidemiology (1938)

R. G. GREEN C. L. Larson

Journal Article A DESCRIPTION OF SHOCK DISEASE IN THE SNOWSHOE HARE Get access R. G. GREEN, R. G. GREEN Search for other works by this author on: Oxford Academic PubMed Google Scholar C. L. LARSON C. L. LARSON Search for other works by this author on: Oxford Academic PubMed Google Scholar American Journal of Epidemiology, Volume 28, Issue 2, September 1938, Pages 190–212, https://doi.org/10.1093/oxfordjournals.aje.a118438 Published: 01 September 1938 Article history Received: 28 May 1938 Published: 01 September 1938

10.1093/oxfordjournals.aje.a118438

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Citations (20)

An Epidemic of a Severe Pneumonitis in the Bayou Region of Louisiana: VI. A Comparative Study of the Viruses of Lymphogranuloma Venereum, Psittacosis, and Louisiana Pneumonitis

Public Health Reports (1896-1970) (1946)

C. L. Larson B. J. Olson

Lymphogranuloma venereum

Psittacosis

Pneumonitis

Ornithosis

10.2307/4585532

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Citations (10)

An Epidemic of a Severe Pneumonitis in the Bayou Region of Louisiana: V. Etiology

Public Health Reports (1896-1970) (1945)

B. J. Olson C. L. Larson

Etiology

10.2307/4585497

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Citations (28)

Noncanonical Inhibition of mTORC1 by Coxiella burnetii Promotes Replication within a Phagolysosome-Like Vacuole

mBio (2019)

C. L. Larson Kelsi M. Sandoz Diane C. Cockrell Robert A. Heinzen

The Q fever agent Coxiella burnetii is a Gram-negative bacterium that invades macrophages and replicates inside a specialized lysosomal vacuole. The pathogen employs a type 4B secretion system (T4BSS) to deliver effector proteins into the host cell that modify the Coxiella-containing vacuole (CCV) into a replication-permissive niche. Mature CCVs are massive degradative organelles that acquire lysosomal proteins. Inhibition of mammalian (or mechanistic) target of rapamycin complex 1 (mTORC1) kinase by nutrient deprivation promotes autophagy and lysosome fusion, as well as activation of the transcription factors TFE3 and TFEB (TFE3/B), which upregulates expression of lysosomal genes. Here, we report that C. burnetii inhibits mTORC1 as evidenced by impaired localization of mTORC1 to endolysosomal membranes and decreased phosphorylation of elF4E-binding protein 1 (4E-BP1) and S6 kinase 1 in infected cells. Infected cells exhibit increased amounts of autophagy-related proteins protein 1A/1B-light chain 3 (LC3) and p62 as well as of activated TFE3. However, C. burnetii did not accelerate autophagy or block autophagic flux triggered by cell starvation. Activation of autophagy or transcription by TFE3/B increased CCV expansion without enhancing bacterial replication. By contrast, knockdown of tuberous sclerosis complex 1 (TSC1) or TSC2, which hyperactivates mTORC1, impaired CCV expansion and bacterial replication. Together, these data demonstrate that specific inhibition of mTORC1 by C. burnetii, but not amplified cell catabolism via autophagy, is required for optimal pathogen replication. These data reveal a complex interplay between lysosomal function and host cell metabolism that regulates C. burnetii intracellular growth.IMPORTANCECoxiella burnetii is an intracellular pathogenic bacterium that replicates within a lysosomal vacuole. Biogenesis of the Coxiella-containing vacuole (CCV) requires effector proteins delivered into the host cell cytosol by the type 4B secretion system (T4BSS). Modifications to lysosomal physiology required for pathogen replication within the CCV are poorly understood. Mammalian (or mechanistic) target of rapamycin complex 1 (mTORC1) is a master kinase that regulates lysosome structure and function. Nutrient deprivation inhibits mTORC1, which promotes cell catabolism in the form of accelerated autophagy and increased lysosome biosynthesis. Here, we report that C. burnetii growth is enhanced by T4BSS-dependent inhibition of mTORC1 that does not activate autophagy. Canonical inhibition of mTORC1 by starvation or inhibitor treatment that induces autophagic flux does not benefit C. burnetii growth. Furthermore, hyperactivation of mTORC1 impairs bacterial replication. These findings indicate that C. burnetii inhibition of mTORC1 without accelerated autophagy promotes bacterial growth.

Coxiella burnetii

TFEB

RHEB

10.1128/mbio.02816-18

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Citations (25)

Essential Role for the Response Regulator PmrA in Coxiella burnetii Type 4B Secretion and Colonization of Mammalian Host Cells

Journal of Bacteriology (2014)

Paul A. Beare Kelsi M. Sandoz C. L. Larson Dale Howe Brent N. Kronmiller

Successful host cell colonization by the Q fever pathogen, Coxiella burnetii, requires translocation of effector proteins into the host cytosol by a Dot/Icm type 4B secretion system (T4BSS). In Legionella pneumophila, the two-component system (TCS) PmrAB regulates the Dot/Icm T4BSS and several additional physiological processes associated with pathogenesis. Because PmrA consensus regulatory elements are associated with some dot/icm and substrate genes, a similar role for PmrA in regulation of the C. burnetii T4BSS has been proposed. Here, we constructed a C. burnetii pmrA deletion mutant to directly probe PmrA-mediated gene regulation. Compared to wild-type bacteria, C. burnetii ΔpmrA exhibited severe intracellular growth defects that coincided with failed secretion of effector proteins. Luciferase gene reporter assays demonstrated PmrA-dependent expression of 5 of 7 dot/icm operons and 9 of 11 effector-encoding genes with a predicted upstream PmrA regulatory element. Mutational analysis verified consensus sequence nucleotides required for PmrA-directed transcription. RNA sequencing and whole bacterial cell mass spectrometry of wild-type C. burnetii and the ΔpmrA mutant uncovered new components of the PmrA regulon, including several genes lacking PmrA motifs that encoded Dot/Icm substrates. Collectively, our results indicate that the PmrAB TCS is a critical virulence factor that regulates C. burnetii Dot/Icm secretion. The presence of PmrA-responsive genes lacking PmrA regulatory elements also suggests that the PmrAB TCS controls expression of regulatory systems associated with the production of additional C. burnetii proteins involved in host cell parasitism.

Coxiella burnetii

Regulon

10.1128/jb.01532-14

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Citations (43)

Quantification of the relative roles of niche and neutral processes in structuring gastrointestinal microbiomes

Proceedings of the National Academy of Sciences (2012)

Patricio Jeraldo Maksim Sipos Nicholas Chia Jennifer M. Brulc A. S. Dhillon

The theoretical description of the forces that shape ecological communities focuses around two classes of models. In niche theory, deterministic interactions between species, individuals, and the environment are considered the dominant factor, whereas in neutral theory, stochastic forces, such as demographic noise, speciation, and immigration, are dominant. Species abundance distributions predicted by the two classes of theory are difficult to distinguish empirically, making it problematic to deduce ecological dynamics from typical measures of diversity and community structure. Here, we show that the fusion of species abundance data with genome-derived measures of evolutionary distance can provide a clear indication of ecological dynamics, capable of quantifying the relative roles played by niche and neutral forces. We apply this technique to six gastrointestinal microbiomes drawn from three different domesticated vertebrates, using high-resolution surveys of microbial species abundance obtained from carefully curated deep 16S rRNA hypervariable tag sequencing data. Although the species abundance patterns are seemingly well fit by the neutral theory of metacommunity assembly, we show that this theory cannot account for the evolutionary patterns in the genomic data; moreover, our analyses strongly suggest that these microbiomes have, in fact, been assembled through processes that involve a significant nonneutral (niche) contribution. Our results demonstrate that high-resolution genomics can remove the ambiguities of process inference inherent in classic ecological measures and permits quantification of the forces shaping complex microbial communities.

Metacommunity

Relative abundance distribution

10.1073/pnas.1206721109

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Citations (148)