The potential role of the gut microbiome on Psoriasis
Samarth Patel (#1390938),
Yousuf Al-qaraghuly (#1390176),
University of Guelph
BIOL*1090 - Intro to Molecular and Cellular Biology
Professor Wijekoon
March 22, 2026
, The gut microbiome is essential in many processes, specifically in regulating immune
responses and balance. In the gastrointestinal (GI) tract, the microorganisms interact with the
body and immune function. Disruptions in the balance, also known as dysbiosis, can lead to
inflammation and immune dysfunction (Alesa et al., 2019). The gut microbiome of psoriasis
patients is distinct from that of healthy individuals (Zhang et al., 2021). Thus, disruptions in the
microbial environment may contribute to the development of psoriasis by altering immune signal
pathways and increasing inflammatory responses associated with psoriasis.
The gut microbiome contains microorganisms that interact closely with the immune
system (Alesa et al., 2019). The microbiome is also key in many biological processes, such as
nutrient metabolism and protection against harmful pathogens (Alesa et al., 2019). The GI tract
holds a significant portion of the body’s immune cells, and interactions between microbes and
immune cells are essential in maintaining immune homeostasis (Alesa et al., 2019). Gut
microbes maintain the balance between T cells and regulatory T cells (Alesa et al., 2019). Some
organisms produce short-chain fatty acids (SCFAs) that support immune activity and increase
anti-inflammatory responses (Alesa et al., 2019). These protect the body from disorders such as
psoriasis (Alesa et al., 2019).
Dysbiosis reduces the expression of junction proteins, increasing intestinal permeability
(Wang et al., 2026). This allows microbial-associated molecular patterns (MAMPs), such as
lipopolysaccharides, to enter circulation (Wang et al., 2026). MAMPs act as danger signals that
can trigger immune responses leading to inflammation (Wang et al., 2026). Furthermore,
immune cell interactions can advance inflammation. Bacteria like Bifidobacterium adolescentis
can activate T-helper 17 cells (Th17) in cell cultures (Wang et al., 2026). Th17 cells secrete
cytokines such as IL-17a and TNF-a which target keratinocytes, the primary cell component of
Samarth Patel (#1390938),
Yousuf Al-qaraghuly (#1390176),
University of Guelph
BIOL*1090 - Intro to Molecular and Cellular Biology
Professor Wijekoon
March 22, 2026
, The gut microbiome is essential in many processes, specifically in regulating immune
responses and balance. In the gastrointestinal (GI) tract, the microorganisms interact with the
body and immune function. Disruptions in the balance, also known as dysbiosis, can lead to
inflammation and immune dysfunction (Alesa et al., 2019). The gut microbiome of psoriasis
patients is distinct from that of healthy individuals (Zhang et al., 2021). Thus, disruptions in the
microbial environment may contribute to the development of psoriasis by altering immune signal
pathways and increasing inflammatory responses associated with psoriasis.
The gut microbiome contains microorganisms that interact closely with the immune
system (Alesa et al., 2019). The microbiome is also key in many biological processes, such as
nutrient metabolism and protection against harmful pathogens (Alesa et al., 2019). The GI tract
holds a significant portion of the body’s immune cells, and interactions between microbes and
immune cells are essential in maintaining immune homeostasis (Alesa et al., 2019). Gut
microbes maintain the balance between T cells and regulatory T cells (Alesa et al., 2019). Some
organisms produce short-chain fatty acids (SCFAs) that support immune activity and increase
anti-inflammatory responses (Alesa et al., 2019). These protect the body from disorders such as
psoriasis (Alesa et al., 2019).
Dysbiosis reduces the expression of junction proteins, increasing intestinal permeability
(Wang et al., 2026). This allows microbial-associated molecular patterns (MAMPs), such as
lipopolysaccharides, to enter circulation (Wang et al., 2026). MAMPs act as danger signals that
can trigger immune responses leading to inflammation (Wang et al., 2026). Furthermore,
immune cell interactions can advance inflammation. Bacteria like Bifidobacterium adolescentis
can activate T-helper 17 cells (Th17) in cell cultures (Wang et al., 2026). Th17 cells secrete
cytokines such as IL-17a and TNF-a which target keratinocytes, the primary cell component of
