 Re: folliculitis
Hi,
Don't have what you have. Have had a few things of short duration that
may have been
similar.
Lets google,
http://dermnetnz.org/acne/scalp-folliculitis.html
http://www.google.com/search?q=necr..ic,12978.0.html
Interesting.
And look at pubmed,
http://www.superarray.com/gene_arra..L/HS-021.2.html
Eotaxins and CCR3 receptor in inflammatory and allergic skin diseases:
therapeutical implications.
Amerio P, Frezzolini A, Feliciani C, Verdolini R, Teofoli P, De Pita O,
Puddu P.
Department of Immunodermatology and Allergology, Istituto Dermopatico
dell' Immacolata-IRCCS, Rome, Italy. p.amerio@idi.it
Cell migration is mediated by a group of chemotactic cytokines called
chemokines: low molecular weight molecules that have been shown as
important leukocyte chemical attractants to sites of inflammation and
infection. Eotaxin-1, also called CCL11, was first described in 1994,
as a highly specific eosinophils chemokine. Many cell types including
lymphocytes, macrophages, bronchial smooth muscle cells, endothelial
cells and eosinophils, are able to produce this chemokine,
predominantly after cytokine stimulation, however little is known about
its expression in human skin in vivo. Eotaxin-1 also regulates the
chemiotaxis and, in some conditions, activation of basophils, mast
cells and T lymphocytes. Chemokine receptors are named from their
ligand families, thus the CC chemokine eotaxin-1 binds to the CCR3
receptor which is expressed on eosinophis, mast cells, Th2 type
lymphocytes and even on keratinocytes. It seems that eotaxin-1 is one
of the most important cytokines involved in tissue inflammation playing
a central role in the pathogenesis of allergic airway diseases (asthma
and rhinitis), in inflammatory bowel disease and gastrointestinal
allergic hypersensitivity and recently it has been proposed as a
therapeutical target for these conditions. Our group has studied the
role of eotaxin-1 in the pathogenesis of two skin conditions:
dermatitis herpetiformis and AIDS-associated eosinophilic folliculitis,
demonstrating that this chemokine, together with Th2 type cytokines
(IL-13 and IL-4) is important in cell recruitment, inflammation and
tissue damage; moreover eotaxin has proven to paly an important role in
other skin conditions such as, bullous pemphigoid, pemphigoid
gestationis, atopic dermatitis and allergic drug reactions Recent
advances in the understanding of eotaxin-1-mediated mechanisms of
chemotaxis in allergic and inflammatory conditions may predict that
therapeutic antagonism is achievable. This paper will focus on the role
that eotaxin and its receptor play in the pathogenetical mechanism in a
number of dermatologic diseases, some of which, like atopic dermatitis,
may benefit from the introduction of novel and more selective
therapeutic options.
Seborrhoeic dermatitis and Pityrosporum (Malassezia) folliculitis:
characterization of inflammatory cells and mediators in the skin by
immunohistochemistry.
Faergemann J, Bergbrant IM, Dohse M, Scott A, Westgate G.
Department of Dermatology, Sahlgrenska university Hospital, S-413 45
Gothenburg, Sweden. jan.faergemann@derm.gu.se
BACKGROUND: The fact that Pityrosporum ovale plays a part in
seborrhoeic dermatitis is well established but the mechanism of this
relationship has not been established. OBJECTIVES: To compare the
number and type of inflammatory cells and mediators in skin biopsies
from normal and lesional skin from the trunk and scalp in patients with
seborrhoeic dermatitis, Pityrosporum (Malassezia) folliculitis and in
normal skin from healthy controls. METHODS: The skin biopsies were
stained using the labelled Streptavidin-biotin METHOD: The following
markers were studied: CD4, CD8, CD68, HLA-DR, NK1, CD16, C1q, C3c, IgG,
CD54 (ICAM-1), interleukin (IL) -1alpha, IL-1beta, IL-2, IL-4, IL-6,
IL-10, IL-12, tumour necrosis factor-alpha and interferon-gamma.
RESULTS: HLA-DR+ cells were seen in the highest number, and were higher
in lesional skin compared with normal skin from both patients and
healthy volunteers. ICAM-1 expression was also increased in lesional
skin. C1q and the interleukins showed an increased cellular and
intercellular staining in patients compared with healthy controls and
the intercellular staining was often more intense in lesions compared
with non-lesional skin. Staining was often more intense when Malassezia
(Pityrosporum ovale) yeast cells were present. CONCLUSIONS: An increase
in NK1+ and CD16+ cells in combination with complement activation
indicates that an irritant non-immunogenic stimulation of the immune
system is important. The result with the interleukins showed both an
increase in the production of inflammatory interleukins as well as in
the regulatory interleukins for both TH1 and TH2 cells. Similarities to
the immune response described for Candida albicans infections indicate
the role of Malassezia in the skin response in seborrhoeic dermatitis
and Pityrosporum folliculitis.
PMID: 11260013
********
I'd say you have a Th2 condition off hand. Similar to seborrhoeic
dermatitis, an atopic condition. P being Th1 doesn't help us to relate
much. We don't have a lack of defensins in the skin, like folks with
atopy.
As you can see in your post to that skin cell thread, the gal who
recovered from it, did
a nutrition program that avoided triggers.
If I were you, i'd get on the good nutrition bandwagon and attempt to
cultivate good flora on the skin.
As to food, this should be good enough.
University of Michigan Food Pyramid
http://www.med.umich.edu/umim/clini..ramid/index.htm
As to whats on the outside, i'd tend to my insides and be very careful
to find some sort of balance that works.
After all you've had a ton of antibiotics and that certainly skews
things.
Finding your way back to the norm won't be easy. Maybe your doctor can
supply
some long shots on this.
Good luck,
randall
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