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KYOTO, JAPAN – Prolactin may be a key mediator in the pathway by which psychological stress triggers and exacerbates psoriasis, Dr. Ewan A. Langan said at an international investigative dermatology meeting.
This raises the intriguing prospect that prolactin may offer a novel future therapeutic target in psoriasis and other skin diseases that worsen in response to psychological distress, said Dr. Langan, who is with the University of Manchester (England).
Prolactin is a “remarkably versatile” neurohormone for which more than 300 distinct biologic actions have been identified. Several of these involve the skin, he noted.
For example, prolactin has been shown to promote keratinocyte proliferation and differentiation, angiogenesis, and a Th1 proinflammatory local cutaneous milieu marked by a T-cell-predominant infiltrate.
These just happen to be among the hallmarks of psoriasis, Dr. Langan observed at the meeting of the European Society for Dermatological Research, the Japanese Society for Investigative Dermatology, and the Society for Investigative Dermatology.
Dr. Langan presented what he described as the first-ever study to demonstrate that prolactin levels and prolactin receptor expression are increased in chronic psoriatic plaques, compared with the normal photo-protected skin of healthy controls.
The study involved 10 patients with early-onset chronic plaque psoriasis and 10 controls, all of whom surrendered skin biopsies that were subsequently analyzed immunohistochemically.
Both prolactin and prolactin receptors were detected in epidermal keratinocytes, dermal fibroblasts, and sweat glands of healthy controls.
By comparison, however, expression of prolactin and prolactin receptors was markedly upregulated throughout the epidermis in psoriasis plaques, especially in the basal layer, probably because of local cutaneous production.
No significant difference was noted between expression in the uninvolved skin of psoriasis patients and samples from normal controls.
The most likely scenario is that prolactin enhances interferon-?-induced chemokine production in keratinocytes, thereby facilitating cutaneous T-cell infiltration, according to Dr. Langan.
Planned future studies will attempt to pin down the factors that regulate cutaneous prolactin and prolactin receptor production, he added.
KYOTO, JAPAN – Prolactin may be a key mediator in the pathway by which psychological stress triggers and exacerbates psoriasis, Dr. Ewan A. Langan said at an international investigative dermatology meeting.
This raises the intriguing prospect that prolactin may offer a novel future therapeutic target in psoriasis and other skin diseases that worsen in response to psychological distress, said Dr. Langan, who is with the University of Manchester (England).
Prolactin is a “remarkably versatile” neurohormone for which more than 300 distinct biologic actions have been identified. Several of these involve the skin, he noted.
For example, prolactin has been shown to promote keratinocyte proliferation and differentiation, angiogenesis, and a Th1 proinflammatory local cutaneous milieu marked by a T-cell-predominant infiltrate.
These just happen to be among the hallmarks of psoriasis, Dr. Langan observed at the meeting of the European Society for Dermatological Research, the Japanese Society for Investigative Dermatology, and the Society for Investigative Dermatology.
Dr. Langan presented what he described as the first-ever study to demonstrate that prolactin levels and prolactin receptor expression are increased in chronic psoriatic plaques, compared with the normal photo-protected skin of healthy controls.
The study involved 10 patients with early-onset chronic plaque psoriasis and 10 controls, all of whom surrendered skin biopsies that were subsequently analyzed immunohistochemically.
Both prolactin and prolactin receptors were detected in epidermal keratinocytes, dermal fibroblasts, and sweat glands of healthy controls.
By comparison, however, expression of prolactin and prolactin receptors was markedly upregulated throughout the epidermis in psoriasis plaques, especially in the basal layer, probably because of local cutaneous production.
No significant difference was noted between expression in the uninvolved skin of psoriasis patients and samples from normal controls.
The most likely scenario is that prolactin enhances interferon-?-induced chemokine production in keratinocytes, thereby facilitating cutaneous T-cell infiltration, according to Dr. Langan.
Planned future studies will attempt to pin down the factors that regulate cutaneous prolactin and prolactin receptor production, he added.
KYOTO, JAPAN – Prolactin may be a key mediator in the pathway by which psychological stress triggers and exacerbates psoriasis, Dr. Ewan A. Langan said at an international investigative dermatology meeting.
This raises the intriguing prospect that prolactin may offer a novel future therapeutic target in psoriasis and other skin diseases that worsen in response to psychological distress, said Dr. Langan, who is with the University of Manchester (England).
Prolactin is a “remarkably versatile” neurohormone for which more than 300 distinct biologic actions have been identified. Several of these involve the skin, he noted.
For example, prolactin has been shown to promote keratinocyte proliferation and differentiation, angiogenesis, and a Th1 proinflammatory local cutaneous milieu marked by a T-cell-predominant infiltrate.
These just happen to be among the hallmarks of psoriasis, Dr. Langan observed at the meeting of the European Society for Dermatological Research, the Japanese Society for Investigative Dermatology, and the Society for Investigative Dermatology.
Dr. Langan presented what he described as the first-ever study to demonstrate that prolactin levels and prolactin receptor expression are increased in chronic psoriatic plaques, compared with the normal photo-protected skin of healthy controls.
The study involved 10 patients with early-onset chronic plaque psoriasis and 10 controls, all of whom surrendered skin biopsies that were subsequently analyzed immunohistochemically.
Both prolactin and prolactin receptors were detected in epidermal keratinocytes, dermal fibroblasts, and sweat glands of healthy controls.
By comparison, however, expression of prolactin and prolactin receptors was markedly upregulated throughout the epidermis in psoriasis plaques, especially in the basal layer, probably because of local cutaneous production.
No significant difference was noted between expression in the uninvolved skin of psoriasis patients and samples from normal controls.
The most likely scenario is that prolactin enhances interferon-?-induced chemokine production in keratinocytes, thereby facilitating cutaneous T-cell infiltration, according to Dr. Langan.
Planned future studies will attempt to pin down the factors that regulate cutaneous prolactin and prolactin receptor production, he added.