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Volume 6, Issue 6(Suppl)
J Clin Toxicol 2016
ISSN: 2161-0495, JCT an open access journal
Page 73
Notes:
Euro Toxicology 2016
October 24-26, 2016
conferenceseries
.com
Toxicology & Applied Pharmacology
October 24-26, 2016 Rome, Italy
7
th
Euro-Global Summit on
Nickel related
Staphylococcus aureus
infections in atopic dermatitis
Anna Magdalena Bogdali
Jagiellonian University Medical College in Krakow, Poland
P
ollution of the air, water and food by metals results in changes of microbiota because metals are common enzymatic
cofactors of bacterial cells. Concentration of nickel in the air in Krakow is approximately 20 ng/m
3
in PM10. Nickel allergy
is often found in patients with atopic dermatitis. Number of colonies of
Staphylococcus aureus
increases in acute phase and
is reduced in remission of atopic dermatitis. Thus, it is believed that staphylococcal-derived infections exacerbate allergic
inflammation. Nickel participates in virulence of
Staphylococcus aureus
and is required as a cofactor for bacterial enzymes
including urease that can regulate pH. It is still unknown whether nickel-sensitive urease can regulate pH of the skin changed
in patients with atopic dermatitis. In our current studies, 85% of patients with atopic dermatitis is infected by difficult to treat
infections by methicillin-resistant
Staphylococcus aureus
. Bacterial infections are initiated by specific adhesion of a bacterium
to the target environment.
Staphylococcus aureus
can attach to nickel nanostructures with dimensions comparable to the size of
a single bacterium. Changes of cytokine milieu due to nickel action on T cells can increase number of immature Th0 and it can
also promote staphylococcal infections because it reduces bacterial clearance. Thus, more immature T cells less cellular immune
mechanisms protecting against staphylococcal infections. Therefore we believe that nickel allergy can promote
Staphylococcus
aureus
infections in atopic dermatitis. All these studies are required to fully understand patho-mechanism of atopic dermatitis
that is useful for more individual and consequently better treatment of patients.
Biography
Anna Magdalena Bogdali graduated with her Master’s degree at the Department of Biochemistry, Biophysics and Biotechnology of Jagiellonian University in
Krakow. She completed her PhD on Atopic Dermatitis from Jagiellonian University Medical College in Medical Biology. She participated in the Socrates/Erasmus
and 6
th
and 7
th
Framework European Programs. She stayed in the Angioedema Hungarian Center at the Semmelweis University in Budapest and she is involved
in projects on hereditary angioedema concerning genetic background and immune mechanisms at the Jagiellonian University Medical College in Krakow. Her
interests are immune and genetics mechanisms mostly related to T cells in the skin and circulatory system.
anna.bogdali@gmail.comAnna Magdalena Bogdali, J Clin Toxicol 2016, 6:6(Suppl)
http://dx.doi.org/10.4172/2161-0495.C1.021