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Joshua Breidenbach
Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, Toledo, OH 43614, USA

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Review
Published: 13 November 2020 in Journal of Clinical Medicine
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The cluster of differentiation 40 (CD40) is activated by the CD40 ligand (CD40L) in a variety of diverse cells types and regulates important processes associated with kidney disease. The CD40/CD40L signaling cascade has been comprehensively studied for its roles in immune functions, whereas the signaling axis involved in local kidney injury has only drawn attention in recent years. Clinical studies have revealed that circulating levels of soluble CD40L (sCD40L) are associated with renal function in the setting of kidney disease. Levels of the circulating CD40 receptor (sCD40), sCD40L, and local CD40 expression are tightly related to renal injury in different types of kidney disease. Additionally, various kidney cell types have been identified as non-professional antigen-presenting cells (APCs) that express CD40 on the cell membrane, which contributes to the interactions between immune cells and local kidney cells during the development of kidney injury. Although the potential for adverse CD40 signaling in kidney cells has been reported in several studies, a summary of those studies focusing on the role of CD40 signaling in the development of kidney disease is lacking. In this review, we describe the outcomes of recent studies and summarize the potential therapeutic methods for kidney disease which target CD40.

ACS Style

Shungang Zhang; Joshua D. Breidenbach; Benjamin H. Russell; Jerrin George; Steven T. Haller. CD40/CD40L Signaling as a Promising Therapeutic Target for the Treatment of Renal Disease. Journal of Clinical Medicine 2020, 9, 3653 .

AMA Style

Shungang Zhang, Joshua D. Breidenbach, Benjamin H. Russell, Jerrin George, Steven T. Haller. CD40/CD40L Signaling as a Promising Therapeutic Target for the Treatment of Renal Disease. Journal of Clinical Medicine. 2020; 9 (11):3653.

Chicago/Turabian Style

Shungang Zhang; Joshua D. Breidenbach; Benjamin H. Russell; Jerrin George; Steven T. Haller. 2020. "CD40/CD40L Signaling as a Promising Therapeutic Target for the Treatment of Renal Disease." Journal of Clinical Medicine 9, no. 11: 3653.

Journal article
Published: 25 September 2020 in Journal of Personalized Medicine
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Viral entry mechanisms for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are an important aspect of virulence. Proposed mechanisms involve host cell membrane-bound angiotensin-converting enzyme 2 (ACE2), type II transmembrane serine proteases (TTSPs), such as transmembrane serine protease isoform 2 (TMPRSS2), lysosomal endopeptidase Cathepsin L (CTSL), subtilisin-like proprotein peptidase furin (FURIN), and even potentially membrane bound heparan sulfate proteoglycans. The distribution and expression of many of these genes across cell types representing multiple organ systems in healthy individuals has recently been demonstrated. However, comorbidities such as diabetes and cardiovascular disease are highly prevalent in patients with Coronavirus Disease 2019 (COVID-19) and are associated with worse outcomes. Whether these conditions contribute directly to SARS-CoV-2 virulence remains unclear. Here, we show that the expression levels of ACE2, TMPRSS2 and other viral entry-related genes, as well as potential downstream effector genes such as bradykinin receptors, are modulated in the target organs of select disease states. In tissues, such as the heart, which normally express ACE2 but minimal TMPRSS2, we found that TMPRSS2 as well as other TTSPs are elevated in individuals with comorbidities compared to healthy individuals. Additionally, we found the increased expression of viral entry-related genes in the settings of hypertension, cancer, or smoking across target organ systems. Our results demonstrate that common comorbidities may contribute directly to SARS-CoV-2 virulence and we suggest new therapeutic targets to improve outcomes in vulnerable patient populations.

ACS Style

Joshua Breidenbach; Prabhatchandra Dube; Subhanwita Ghosh; Belal Abdullah; Nikolai Modyanov; Deepak Malhotra; Lance Dworkin; Steven Haller; David Kennedy. Impact of Comorbidities on SARS-CoV-2 Viral Entry-Related Genes. Journal of Personalized Medicine 2020, 10, 146 .

AMA Style

Joshua Breidenbach, Prabhatchandra Dube, Subhanwita Ghosh, Belal Abdullah, Nikolai Modyanov, Deepak Malhotra, Lance Dworkin, Steven Haller, David Kennedy. Impact of Comorbidities on SARS-CoV-2 Viral Entry-Related Genes. Journal of Personalized Medicine. 2020; 10 (4):146.

Chicago/Turabian Style

Joshua Breidenbach; Prabhatchandra Dube; Subhanwita Ghosh; Belal Abdullah; Nikolai Modyanov; Deepak Malhotra; Lance Dworkin; Steven Haller; David Kennedy. 2020. "Impact of Comorbidities on SARS-CoV-2 Viral Entry-Related Genes." Journal of Personalized Medicine 10, no. 4: 146.

Journal article
Published: 08 June 2020 in Toxins
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Harmful algal blooms (HAB) have become a major health concern worldwide, not just to humans that consume and recreate on contaminated waters, but also to the fauna that inhabit the environments surrounding affected areas. HABs contain heterotrophic bacteria, cyanobacterial lipopolysaccharide, and cyanobacterial toxins such as microcystins, that can cause severe toxicity in many aquatic species as well as bioaccumulation within various organs. Thus, the possibility of trophic transference of this toxin through the food chain has potentially important health implications for other organisms in the related food web. While some species have developed adaptions to attenuate the toxic effects of HAB toxins, there are still numerous species that remain vulnerable, including Lithobates catesbeiana (American bullfrog) tadpoles. In the current study we demonstrate that acute, short-term exposure of tadpoles to HAB toxins containing 1 µg/L (1 nmol/L) of total microcystins for only 7 days results in significant liver and intestinal toxicity within tadpoles. Exposed tadpoles had increased intestinal diameter, decreased intestinal fold heights, and a constant number of intestinal folds, indicating pathological intestinal distension, similar to what is seen in various disease processes, such as toxic megacolon. HAB-toxin-exposed tadpoles also demonstrated hepatocyte hypertrophy with increased hepatocyte binucleation consistent with carcinogenic and oxidative processes within the liver. Both livers and intestines of HAB-toxin-exposed tadpoles demonstrated significant increases in protein carbonylation consistent with oxidative stress and damage. These findings demonstrate that short-term exposure to HAB toxins, including microcystins, can have significant adverse effects in amphibian populations. This acute, short-term toxicity highlights the need to evaluate the influence HAB toxins may have on other vulnerable species within the food web and how those may ultimately also impact human health.

ACS Style

Robin C. Su; Casey M. Meyers; Emily A. Warner; Jessica A. Garcia; Jeanine M. Refsnider; Apurva Lad; Joshua D. Breidenbach; Nikolai Modyanov; Deepak Malhotra; Steven T. Haller; David J. Kennedy. Harmful Algal Bloom Toxicity in Lithobates catesbeiana Tadpoles. Toxins 2020, 12, 378 .

AMA Style

Robin C. Su, Casey M. Meyers, Emily A. Warner, Jessica A. Garcia, Jeanine M. Refsnider, Apurva Lad, Joshua D. Breidenbach, Nikolai Modyanov, Deepak Malhotra, Steven T. Haller, David J. Kennedy. Harmful Algal Bloom Toxicity in Lithobates catesbeiana Tadpoles. Toxins. 2020; 12 (6):378.

Chicago/Turabian Style

Robin C. Su; Casey M. Meyers; Emily A. Warner; Jessica A. Garcia; Jeanine M. Refsnider; Apurva Lad; Joshua D. Breidenbach; Nikolai Modyanov; Deepak Malhotra; Steven T. Haller; David J. Kennedy. 2020. "Harmful Algal Bloom Toxicity in Lithobates catesbeiana Tadpoles." Toxins 12, no. 6: 378.

Journal article
Published: 02 June 2020 in Biomedicines
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Inflammatory Bowel Disease (IBD) is one of the most common gastrointestinal (GI) disorders around the world, and includes diagnoses such as Crohn’s disease and ulcerative colitis. The etiology of IBD is influenced by genetic and environmental factors. One environmental perturbagen that is not well studied within the intestines is microcystin-leucine arginine (MC-LR), which is a toxin produced by cyanobacteria in freshwater environments around the world. We recently reported that MC-LR has limited effects within the intestines of healthy mice, yet interestingly has significant toxicity within the intestines of mice with pre-existing colitis induced by dextran sulfate sodium (DSS). MC-LR was found to prolong DSS-induced weight loss, prolong DSS-induced bloody stools, exacerbate DSS-induced colonic shortening, exacerbate DSS-induced colonic ulceration, and exacerbate DSS-induced inflammatory cytokine upregulation. In addition, we previously reported a significant increase in expression of the pro-inflammatory receptor CD40 in the colons of these mice, along with downstream products of CD40 activation, including plasminogen activator inhibitor-1 (PAI-1) and monocyte chemoattractant protein-1 (MCP-1). In the current study, we demonstrate that knocking out CD40 attenuates the effects of MC-LR in mice with pre-existing colitis by decreasing the severity of weight loss, allowing a full recovery in bloody stools, preventing the exacerbation of colonic shortening, preventing the exacerbation of colonic ulceration, and preventing the upregulation of the pro-inflammatory and pro-fibrotic cytokines IL-1β, MCP-1, and PAI-1. We also demonstrate the promising efficacy of a CD40 receptor blocking peptide to ameliorate the effects of MC-LR exposure in a proof-of-concept study. Our findings suggest for the first time that MC-LR acts through a CD40-dependent mechanism to exacerbate colitis.

ACS Style

Robin C. Su; Emily A. Warner; Joshua D. Breidenbach; Apurva Lad; Thomas M. Blomquist; Andrew L. Kleinhenz; Nikolai Modyanov; Deepak Malhotra; David J. Kennedy; Steven T. Haller. CD40 Receptor Knockout Protects against Microcystin-LR (MC-LR) Prolongation and Exacerbation of Dextran Sulfate Sodium (DSS)-Induced Colitis. Biomedicines 2020, 8, 149 .

AMA Style

Robin C. Su, Emily A. Warner, Joshua D. Breidenbach, Apurva Lad, Thomas M. Blomquist, Andrew L. Kleinhenz, Nikolai Modyanov, Deepak Malhotra, David J. Kennedy, Steven T. Haller. CD40 Receptor Knockout Protects against Microcystin-LR (MC-LR) Prolongation and Exacerbation of Dextran Sulfate Sodium (DSS)-Induced Colitis. Biomedicines. 2020; 8 (6):149.

Chicago/Turabian Style

Robin C. Su; Emily A. Warner; Joshua D. Breidenbach; Apurva Lad; Thomas M. Blomquist; Andrew L. Kleinhenz; Nikolai Modyanov; Deepak Malhotra; David J. Kennedy; Steven T. Haller. 2020. "CD40 Receptor Knockout Protects against Microcystin-LR (MC-LR) Prolongation and Exacerbation of Dextran Sulfate Sodium (DSS)-Induced Colitis." Biomedicines 8, no. 6: 149.

Preprint content
Published: 27 May 2020
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Viral entry mechanisms for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are an important aspect of virulence. Proposed mechanisms involve host cell membrane-bound angiotensin-converting enzyme 2 (ACE2) and type II transmembrane serine proteases (TTSPs), such as transmembrane serine protease isoform 2 (TMPRSS2). The distribution of expression of these genes across cell types representing multiple organ systems in healthy individuals has been recently demonstrated. However, comorbidities such as diabetes and cardiovascular disease are highly prevalent in patients with Coronavirus Disease 2019 (COVID-19) and associated with worse outcomes. Whether these conditions contribute directly to SARS-CoV-2 virulence remain unclear. Here we show that the expression levels of ACE2, TMPRSS2 and other viral entry-related genes are modulated in target organs of select disease states. In tissues such as heart, which normally express ACE2 but minimal TMPRSS2, we found that TMPRSS2 as well as other TTSPs are elevated in individuals with comorbidities vs healthy individuals. Additionally, we found increased expression of viral entry-related genes in the settings of hypertension, cancer or smoking across target organ systems. Our results demonstrate that common comorbidities may contribute directly to SARS-CoV-2 virulence and suggest new therapeutic targets to improve outcomes in vulnerable patient populations.

ACS Style

Joshua D. Breidenbach; Prabhatchandra Dube; Subhanwita Ghosh; Nikolai N. Modyanov; Deepak Malhotra; Lance D. Dworkin; Steven T. Haller; David J. Kennedy. Impact of Comorbidities on SARS-CoV-2 Viral Entry-Related Genes. 2020, 1 .

AMA Style

Joshua D. Breidenbach, Prabhatchandra Dube, Subhanwita Ghosh, Nikolai N. Modyanov, Deepak Malhotra, Lance D. Dworkin, Steven T. Haller, David J. Kennedy. Impact of Comorbidities on SARS-CoV-2 Viral Entry-Related Genes. . 2020; ():1.

Chicago/Turabian Style

Joshua D. Breidenbach; Prabhatchandra Dube; Subhanwita Ghosh; Nikolai N. Modyanov; Deepak Malhotra; Lance D. Dworkin; Steven T. Haller; David J. Kennedy. 2020. "Impact of Comorbidities on SARS-CoV-2 Viral Entry-Related Genes." , no. : 1.

Research article
Published: 05 December 2019 in PLOS ONE
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Non-alcoholic fatty liver disease (NAFLD) is a growing global health concern. With a propensity to progress towards non-alcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma, NAFLD is an important link amongst a multitude of comorbidities including obesity, diabetes, and cardiovascular and kidney disease. As several in vivo models of hyperglycemia and NAFLD are employed to investigate the pathophysiology of this disease process, we aimed to characterize an in vitro model of hyperglycemia that was amenable to address molecular mechanisms and therapeutic targets at the cellular level. Utilizing hyperglycemic cell culturing conditions, we induced steatosis within a human hepatocyte cell line (HepG2 cells), as confirmed by electron microscopy. The deposition and accumulation of lipids within hyperglycemic HepG2 cells is significantly greater than in normoglycemic cells, as visualized and quantified by Nile red staining. Alanine aminotransferase (ALT) and alkaline phosphatase (ALP), diagnostic biomarkers for liver damage and disease, were found to be upregulated in hyperglycemic HepG2 cells as compared with normoglycemic cells. Suppression of CEACAM1, GLUT2, and PON1, and elevation of CD36, PCK1, and G6PK were also found to be characteristic in hyperglycemic HepG2 cells compared with normoglycemic cells, suggesting insulin resistance and NAFLD. These in vitro findings mirror the characteristic genetic and phenotypic profile seen in Leprdb/J mice, a well-established in vivo model of NAFLD. In conclusion, we characterize an in vitro model displaying several key genetic and phenotypic characteristics in common with NAFLD that may assist future studies in addressing the molecular mechanisms and therapeutic targets to combat this disease.

ACS Style

Robin C. Su; Apurva Lad; Joshua D. Breidenbach; Thomas M. Blomquist; William T. Gunning; Prabhatchandra Dube; Andrew L. Kleinhenz; Deepak Malhotra; Steven T. Haller; David J. Kennedy. Hyperglycemia induces key genetic and phenotypic changes in human liver epithelial HepG2 cells which parallel the Leprdb/J mouse model of non-alcoholic fatty liver disease (NAFLD). PLOS ONE 2019, 14, e0225604 .

AMA Style

Robin C. Su, Apurva Lad, Joshua D. Breidenbach, Thomas M. Blomquist, William T. Gunning, Prabhatchandra Dube, Andrew L. Kleinhenz, Deepak Malhotra, Steven T. Haller, David J. Kennedy. Hyperglycemia induces key genetic and phenotypic changes in human liver epithelial HepG2 cells which parallel the Leprdb/J mouse model of non-alcoholic fatty liver disease (NAFLD). PLOS ONE. 2019; 14 (12):e0225604.

Chicago/Turabian Style

Robin C. Su; Apurva Lad; Joshua D. Breidenbach; Thomas M. Blomquist; William T. Gunning; Prabhatchandra Dube; Andrew L. Kleinhenz; Deepak Malhotra; Steven T. Haller; David J. Kennedy. 2019. "Hyperglycemia induces key genetic and phenotypic changes in human liver epithelial HepG2 cells which parallel the Leprdb/J mouse model of non-alcoholic fatty liver disease (NAFLD)." PLOS ONE 14, no. 12: e0225604.

Research article
Published: 22 November 2019 in PLOS ONE
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IL-21 is the most recently discovered common gamma-chain cytokine that promotes persistent T-cell responses in chronic infections, autoimmunity and cancer. However, the therapeutic potential of inhibiting the IL-21-BATF signaling axis, particularly in transplant rejection, remains unclear. We used heart transplant models to examine the effects of IL-21 blockade in prevention of chronic cardiac allograft vasculopathy (CAV) using genetic knock-out and therapeutic approaches. Both wild-type C57BL/6 and IL-21-/- strains acutely rejected Balb/c skin grafts and once immunized with this skin graft, rejected Balb/c heart allografts in an accelerated fashion. However, when transplanted with heart grafts from the class-II major histocompatibility complex mutant, B6bm12 mice; wild-type recipients developed CAV, while IL-21-/- recipients were protected, even at day 100 post-transplant. Similarly, BATF-/- recipients, lacking the transcription factor BATF responsible for IL-21 production, did not develop CAV in B6-bm12 heart allografts. Strikingly, in a transient treatment protocol, the development of CAV in wild-type recipients of B6-bm12 hearts allografts was blocked by the administration of IL-21 receptor fusion protein (R-Fc). Thus, we demonstrate that CAV is regulated at least in part by IL-21 signaling and its blockade by genetic approaches or therapy with IL-21R-Fc prevents CAV in mice.

ACS Style

Mithun Khattar; Caitlin E. Baum; Paul Schroder; Joshua D. Breidenbach; Steven T. Haller; Wenhao Chen; Stanislaw Stepkowski. Interleukin 21 (IL-21) regulates chronic allograft vasculopathy (CAV) in murine heart allograft rejection. PLOS ONE 2019, 14, e0225624 .

AMA Style

Mithun Khattar, Caitlin E. Baum, Paul Schroder, Joshua D. Breidenbach, Steven T. Haller, Wenhao Chen, Stanislaw Stepkowski. Interleukin 21 (IL-21) regulates chronic allograft vasculopathy (CAV) in murine heart allograft rejection. PLOS ONE. 2019; 14 (11):e0225624.

Chicago/Turabian Style

Mithun Khattar; Caitlin E. Baum; Paul Schroder; Joshua D. Breidenbach; Steven T. Haller; Wenhao Chen; Stanislaw Stepkowski. 2019. "Interleukin 21 (IL-21) regulates chronic allograft vasculopathy (CAV) in murine heart allograft rejection." PLOS ONE 14, no. 11: e0225624.

Journal article
Published: 23 August 2019 in Toxins
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Microcystins are potent hepatotoxins that have become a global health concern in recent years. Their actions in at-risk populations with pre-existing liver disease is unknown. We tested the hypothesis that the No Observed Adverse Effect Level (NOAEL) of Microcystin-LR (MC-LR) established in healthy mice would cause exacerbation of hepatic injury in a murine model (Leprdb/J) of Non-alcoholic Fatty Liver Disease (NAFLD). Ten-week-old male Leprdb/J mice were gavaged with 50 μg/kg, 100 μg/kg MC-LR or vehicle every 48 h for 4 weeks (n = 15–17 mice/group). Early mortality was observed in both the 50 μg/kg (1/17, 6%), and 100 μg/kg (3/17, 18%) MC-LR exposed mice. MC-LR exposure resulted in significant increases in circulating alkaline phosphatase levels, and histopathological markers of hepatic injury as well as significant upregulation of genes associated with hepatotoxicity, necrosis, nongenotoxic hepatocarcinogenicity and oxidative stress response. In addition, we observed exposure dependent changes in protein phosphorylation sites in pathways involved in inflammation, immune function, and response to oxidative stress. These results demonstrate that exposure to MC-LR at levels that are below the NOAEL established in healthy animals results in significant exacerbation of hepatic injury that is accompanied by genetic and phosphoproteomic dysregulation in key signaling pathways in the livers of NAFLD mice.

ACS Style

Apurva Lad; Robin C. Su; Joshua D. Breidenbach; Paul M. Stemmer; Nicholas J. Carruthers; Nayeli K. Sanchez; Fatimah K. Khalaf; Shungang Zhang; Andrew L. Kleinhenz; Prabhatchandra Dube; Chrysan J. Mohammed; Judy A. Westrick; Erin L. Crawford; Dilrukshika Palagama; David Baliu-Rodriguez; Dragan Isailovic; Bruce Levison; Nikolai Modyanov; Amira F. Gohara; Deepak Malhotra; Steven T. Haller; David J. Kennedy. Chronic Low Dose Oral Exposure to Microcystin-LR Exacerbates Hepatic Injury in a Murine Model of Non-Alcoholic Fatty Liver Disease. Toxins 2019, 11, 486 .

AMA Style

Apurva Lad, Robin C. Su, Joshua D. Breidenbach, Paul M. Stemmer, Nicholas J. Carruthers, Nayeli K. Sanchez, Fatimah K. Khalaf, Shungang Zhang, Andrew L. Kleinhenz, Prabhatchandra Dube, Chrysan J. Mohammed, Judy A. Westrick, Erin L. Crawford, Dilrukshika Palagama, David Baliu-Rodriguez, Dragan Isailovic, Bruce Levison, Nikolai Modyanov, Amira F. Gohara, Deepak Malhotra, Steven T. Haller, David J. Kennedy. Chronic Low Dose Oral Exposure to Microcystin-LR Exacerbates Hepatic Injury in a Murine Model of Non-Alcoholic Fatty Liver Disease. Toxins. 2019; 11 (9):486.

Chicago/Turabian Style

Apurva Lad; Robin C. Su; Joshua D. Breidenbach; Paul M. Stemmer; Nicholas J. Carruthers; Nayeli K. Sanchez; Fatimah K. Khalaf; Shungang Zhang; Andrew L. Kleinhenz; Prabhatchandra Dube; Chrysan J. Mohammed; Judy A. Westrick; Erin L. Crawford; Dilrukshika Palagama; David Baliu-Rodriguez; Dragan Isailovic; Bruce Levison; Nikolai Modyanov; Amira F. Gohara; Deepak Malhotra; Steven T. Haller; David J. Kennedy. 2019. "Chronic Low Dose Oral Exposure to Microcystin-LR Exacerbates Hepatic Injury in a Murine Model of Non-Alcoholic Fatty Liver Disease." Toxins 11, no. 9: 486.

Journal article
Published: 25 June 2019 in Toxins
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Inflammatory Bowel Disease (IBD) represents a collection of gastrointestinal disorders resulting from genetic and environmental factors. Microcystin-leucine arginine (MC-LR) is a toxin produced by cyanobacteria during algal blooms and demonstrates bioaccumulation in the intestinal tract following ingestion. Little is known about the impact of MC-LR ingestion in individuals with IBD. In this study, we sought to investigate MC-LR's effects in a dextran sulfate sodium (DSS)-induced colitis model. Mice were separated into four groups: (a) water only (control), (b) DSS followed by water (DSS), (c) water followed by MC-LR (MC-LR), and (d) DSS followed by MC-LR (DSS + MC-LR). DSS resulted in weight loss, splenomegaly, and severe colitis marked by transmural acute inflammation, ulceration, shortened colon length, and bloody stools. DSS + MC-LR mice experienced prolonged weight loss and bloody stools, increased ulceration of colonic mucosa, and shorter colon length as compared with DSS mice. DSS + MC-LR also resulted in greater increases in pro-inflammatory transcripts within colonic tissue (TNF-α, IL-1β, CD40, MCP-1) and the pro-fibrotic marker, PAI-1, as compared to DSS-only ingestion. These findings demonstrate that MC-LR exposure not only prolongs, but also worsens the severity of pre-existing colitis, strengthening evidence of MC-LR as an under-recognized environmental toxin in vulnerable populations, such as those with IBD.

ACS Style

Robin C. Su; Thomas M. Blomquist; Andrew L. Kleinhenz; Fatimah K. Khalaf; Prabhatchandra Dube; Apurva Lad; Joshua D. Breidenbach; Chrysan J. Mohammed; Shungang Zhang; Caitlin E. Baum; Deepak Malhotra; David J. Kennedy; Steven T. Haller. Exposure to the Harmful Algal Bloom (HAB) Toxin Microcystin-LR (MC-LR) Prolongs and Increases Severity of Dextran Sulfate Sodium (DSS)-Induced Colitis. Toxins 2019, 11, 371 .

AMA Style

Robin C. Su, Thomas M. Blomquist, Andrew L. Kleinhenz, Fatimah K. Khalaf, Prabhatchandra Dube, Apurva Lad, Joshua D. Breidenbach, Chrysan J. Mohammed, Shungang Zhang, Caitlin E. Baum, Deepak Malhotra, David J. Kennedy, Steven T. Haller. Exposure to the Harmful Algal Bloom (HAB) Toxin Microcystin-LR (MC-LR) Prolongs and Increases Severity of Dextran Sulfate Sodium (DSS)-Induced Colitis. Toxins. 2019; 11 (6):371.

Chicago/Turabian Style

Robin C. Su; Thomas M. Blomquist; Andrew L. Kleinhenz; Fatimah K. Khalaf; Prabhatchandra Dube; Apurva Lad; Joshua D. Breidenbach; Chrysan J. Mohammed; Shungang Zhang; Caitlin E. Baum; Deepak Malhotra; David J. Kennedy; Steven T. Haller. 2019. "Exposure to the Harmful Algal Bloom (HAB) Toxin Microcystin-LR (MC-LR) Prolongs and Increases Severity of Dextran Sulfate Sodium (DSS)-Induced Colitis." Toxins 11, no. 6: 371.