Challenges of concurrent HIV infection in the course and management of Crohn's disease

Abstract

Crohn's disease (CD) is a chronic transmural bowel inflammation with a multifactorial etiology involving genetic predisposition and immune dysregulation in response to environmental triggers. In patients with human immunodeficiency virus (HIV), an already compromised immune system further complicates the progression and management of CD, creating unique therapeutic challenges. Probiotics have recently gained attention as a potential therapeutic option for CD, especially due to their role in modulating the gut microbiota. However, their effectiveness in patients with HIV, especially in enhancing and maintaining remissions, remains underexplored. This review aimed to examine how HIV infection influences the course of inflammatory bowel disease (IBD) and its impact on CD management strategies. A systematic literature search was conducted using Google Scholar, PubMed, Springer, and Web of Science to identify studies on patients with HIV and CD. HIV infection significantly alters the progression and management of CD due to its impact on the immune system. The immunosuppressed state of patients with HIV can complicate both the diagnosis and treatment of CD, often requiring adjustments in therapeutic approaches, necessitating a careful, tailored approach.

Keywords: AAD, Antibiotic-Associated Diarrhea; AIDS, Acquired Immunodeficiency Syndrome; AIEC, Adherent-Invasive Escherichia Coli; APC, Antigen-Presenting Cells; ART, Antiretroviral Therapy; CARD15, Caspase Recruitment Domain–Containing Protein 15; CARD9, Caspase Recruitment Domain–Containing Protein 9; CAZymes, Carbohydrate-Active Enzymes; CCL4, C-C Motif Chemokine Ligand 4; CCR5, C-C Chemokine Receptor Type 5; CD, Cluster Of Differentiation; CD, Crohn’s Disease; CRC, Colorectal Cancer; CXCR4, C-X-C Chemokine Receptor Type 4; Crohn’s disease; DC, Dendritic Cells; DC-SIGN, Dendritic Cell–Specific Intercellular Adhesion Molecule-3–Grabbing Non-Integrin; ERS, Endoplasmic Reticulum Stress; FMT, Fecal Microbiota Transplantation; FVT, Fecal Virome Transplantation; GIT, Gastrointestinal Tract; HIV; HIV, Human Immunodeficiency Virus; IBD, Inflammatory Bowel Disease; IFABP, Intestinal Fatty Acid–Binding Protein; IL, Interleukin; ILCs, Innate Lymphoid Cells; MALT, Mucosa-Associated Lymphoid Tissue; MAMP, Microbe-Associated Molecular Pattern; NF-κB, Nuclear Factor Kappa B; NK, Natural Killer Cells; NOD2, Nucleotide-Binding Oligomerization Domain–Containing Protein 2; NOS, Nitric Oxide Synthase; PPAR-γ, Peroxisome Proliferator-Activated Receptor Gamma; PRR, Pattern Recognition Receptor; SCFA, Short-Chain Fatty Acids; SLE, Systemic Lupus Erythematosus; TGF-β, Transforming Growth Factor–β; TLR, Toll-Like Receptor; TNF-α, Tumor Necrosis Factor–α; Th17, T Helper 17 Cells; UC, Ulcerative Colitis; gut microbiota; pDC, Plasmacytoid Dendritic Cells; probiotics; sCD14, Soluble CD14.

Figure 1

Pathogenesis of CD CD, Crohn's Disease; NOD2, Nucleotide-Binding Oligomerization Domain-Containing Protein 2; CARD15, Caspase Recruitment Domain-Containing Protein 15; DC, Dendritic Cells; TNF-α, Tumor Necrosis Factor-Alpha; IL, Interleukin

Figure 2

Gastrointestinal tract dysfunctions in patients with HIV

Figure 3

Medical treatment options for CD