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Published on: June 30, 2022
The neurological significance of abnormal natural killer cell activity in chronic toxigenic mold exposures
Ebere Anyanwu1, Andrew W Campbell, Joseph Jones
1Neurosciences Research, Cahers Inc., Conroe, TX, USA. ebereanyanwu@msn.com
Abstract:
Toxigenic mold activities produce metabolites that are either broad-spectrum antibiotics or mycotoxins that are cytotoxic. Indoor environmental exposure to these toxigenic molds leads to adverse health conditions with the main outcome measure of frequent neuroimmunologic and behavioral consequences. One of the immune system disorders found in patients presenting with toxigenic mold exposure is an abnormal natural killer cell activity. This paper presents an overview of the neurological significance of abnormal natural killer cell (NKC) activity in chronic toxigenic mold exposure. A comprehensive review of the literature was carried out to evaluate and assess the conditions under which the immune system could be dysfunctionally interfered with leading to abnormal NKC activity and the involvement of mycotoxins in these processes. The functions, mechanism, the factors that influence NKC activities, and the roles of mycotoxins in NKCs were cited wherever necessary. The major presentations are headache, general debilitating pains, nose bleeding, fevers with body temperatures up to 40 degrees C (104 degrees F), cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, vertigo/dizziness, and in some cases, seizures. Although sleep is commonly considered a restorative process that is important for the proper functioning of the immune system, it could be disturbed by mycotoxins. Most likely, mycotoxins exert some rigorous effects on the circadian rhythmic processes resulting in sleep deprivation to which an acute and transient increase in NKC activity is observed. Depression, psychological stress, tissue injuries, malignancies, carcinogenesis, chronic fatigue syndrome, and experimental allergic encephalomyelitis could be induced at very low physiological concentrations by mycotoxin-induced NKC activity. In the light of this review, it is concluded that chronic exposures to toxigenic mold could lead to abnormal NKC activity with a wide range of neurological consequences, some of which were headache, general debilitating pains, fever, cough, memory loss, depression, mood swings, sleep disturbances, anxiety, chronic fatigue, and seizures.
Insights
Toxigenic mold exposure can cause abnormal natural killer cell (NKC) activity, leading to neurological and behavioral issues. Mycotoxins disrupt immune function and circadian rhythms, impacting sleep and overall health.
Area of Science:
- Neuroimmunology
- Environmental Health
- Toxicology
Background:
- Toxigenic molds produce mycotoxins, which can be cytotoxic or antibiotic.
- Indoor mold exposure is linked to adverse health effects, particularly neuroimmunologic and behavioral consequences.
- Abnormal natural killer cell (NKC) activity is observed in individuals exposed to toxigenic molds.
Purpose of the Study:
- To review the neurological significance of abnormal NKC activity in chronic toxigenic mold exposure.
- To assess how mycotoxins interfere with immune function and NKC activity.
- To explore the link between mycotoxins, circadian rhythms, and neurological symptoms.
Main Methods:
- Comprehensive literature review.
- Evaluation of immune system dysfunction due to mycotoxins.
- Analysis of factors influencing NKC activity and mycotoxin roles.
Main Results:
- Chronic toxigenic mold exposure can lead to abnormal NKC activity.
- Mycotoxins can disrupt circadian rhythms, affecting sleep and increasing NKC activity.
- Abnormal NKC activity is associated with various neurological symptoms, including fatigue, mood swings, and seizures.
Conclusions:
- Chronic toxigenic mold exposure is linked to abnormal NKC activity.
- Mycotoxins play a significant role in immune dysfunction and neurological consequences.
- Understanding NKC activity is crucial for managing health issues related to mold exposure.
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