IMPORTANT FUNCTIONS OF PROTEINS

a.) Growth and maintenance

 For muscle mass and repair
b.) Biochemical reactions
 Enzymes = biological catalysts, speeds up reactions
 Most likely proteins in nature
c.) Messengers
 Hormones (Testosterone and Estrogen)
d.) Structural
 Helps with the integrity of the cell (Ex: Integral Protein)
 Facilitates the in and out of solutes
 Proteins act as channels and gates
e.) Maintains pH
 Amino acids (acidic, basic, polar, non-polar)
 Acidic and basic – can maintain neutrality of the body, have hydroxyl ions
 Basic protein – can be added if the urine is acidic
f.) Balance fluid
 Osmosis
g.) Immunity
 Antibodies, antigen, t cells, b cells, memory cells, ect.
h.) Transportation
 Helps with the integrity of the cell (Ex: Integral Protein) 
 Same with the structural function
i.) Provides Energy
 Energy source = food (egg, meat)

IMMUNITY

- Active (always on)  ability of an organism to resist infectious disease.

- ability of humans and plants (but different from the vertebrates)
- Infections can be from = pathogens: bacteria, fungi, parasites, or viruses.

LINE OF DEFENSES

1. 1st Line of Defense

o Skin + secretion

 Sweat has enzyme that can kill bacteria on the surface of the skin; Lysozyme is
a naturally occurring enzyme which is found in body secretions. It plays an
important role in the prevention of bacterial infections.

o Mucous membranes + secretion

 Found in the linings of intestine, lungs, nose, upper and lower respiratory tract

 Secrete mucoid substance which traps foreign bodies

 o Microbiome

 Are not always pathogenic or cause disease

 Microbes naturally found in the body are: 

o Skin: Staphylococcus aureus, Micrococcus luteus (normal flora of the
skin)

 Inside the gut is where we can find the most dense population of
microorganism
 The first line of defense can be penetrated by pathogens

NORMAL FLORA OF THE INTESTINE

 Lactobacillus – found in fermented foods; boosts the immunity

 Bacillus – under lactobacillus
 Escherichia coli – if the immune cells are weak, the E. Coli in the body
can turn against you (for the immunocompromised patients)

2. 2nd Line of Defense

 Phagocytic leukocytes – phagocytes (e.g. macrophages and dendritic

cells)
 Antimicrobial proteins – can be secreted by the body or microbiomes
 Inflammatory response – immune cells will rush when there is infection
 Fever – it means that the immune system is fighting well because they
are fighting against infection

3. 3rd line of defense

 Lymphocytes – B cells and t cells
 Antibodies
o Produced by plasma cells which are derived from B cells
o B cells can differentiate into memory cells during infection
 Memory Cell- Cells that can recognize the previous infection. 

LYMPHATIC  SYSTEM

 Transports lymph fluids that contain the immune cells

 This system includes the bone marrow, spleen, thymus, lymph nodes, and lymphatic
veins.
 Primary lymphoid organs (bone marrow and thymus)
 B cells differentiate in the bone marrow
 T cells differentiate in the thymus
 Lymph nodes are found in the armpits, inguinal area and neck
 Secondary lymphoid organs (lymph nodes, spleen and MALT) = Police stations
o Sites where antigen interact with APC phagocytes and lymphocytes for adaptive
immune response
 APCs or Antigen-presenting cell (e.g. macrophages, dendritic cells, and B cells) can
induce immune response
 Antigens – they trigger immune response; found in the body; no antigen = no
pathogen; molecules that act like an id specific to the current pathogen; takes time to be
detected
o Spike proteins act as antigen or surface protein
 Monocytes – WBC that contain many lysozyme and differentiate into macrophages
(macrophages- can undergo phagocytosis)
 Granulocytes – WBC with granules (proteins)
Examples:
 Neutrophils – most abundant during infection
 Basophil – responsible for allergies (inhaling a pollen from a flower, the pollen
will be recognized by the basophil as foreign body)
 Eusinophils – attack parasites (high levels means you have parasitic attack)
 Lymphocytes – involved in adaptive response

 Stem cells – can differentiate into lymphoid and myeloid cells (immune cells); can
differentiate into any kind of cell
o produced in the bone marrow

LYMPHOID CELLS
 if stem cell differentiates into a lymphoid precursor, the lymphoid precursor, if
directly transported in the bone marrow, they can mature as B cell
 if transported in the thymus, they can mature in the thymus as T cell
 B cells can differentiate into plasma to produce antibodies and can also form
memory cells with antibodies specific to the infection or pathogen
 stem cells can be injected in the eyes if there is an eye defect; also in the liver
so it can evolve into liver cells

MYELOID CELLS
 can either differentiate into:
o Monocyte – can be either dendritic cell and macrophages (can undergo
phagocytosis)
have lysozymes because they engulf pathogens
the lysozyme digests the pathogens)
o Granulocyte (mast cell and neutrophils)

FUNCTIONS OF LYMPHATIC SYSTEM

 Body's 'sewerage system'.
 It maintains fluid levels in our body tissues by removing all fluids that leak out of our
blood vessels.
 Important for the optimal functioning of our general and specific immune .
 THE ORIGINS OF IMMUNE RESPONSE CELLS

-Immune response cells develop from pluripotent stem cells in the bone marrow into one
of two immune cell progenitors. Myeloid precursors create monocytes and granulocytes.
Monocytes grow into macrophages or dendritic cells, which are antigen uptake and presentation
cells as well as phagocytic cells. Granulocytes include phosphocytic neutrophils, commonly
known as polymorphonuclear leukocytes or PMNs, and granule-releasing mast cells.
Lymphocytic progenitors create T and B cells, which are lymphocytes that participate directly in
the adaptive immune response. Plasma cells, which are formed from B cells, produce
antibodies.

      IMMUNITY

                      Innate immunity                        Adaptive immunity 

 The non-inducible ability to recognize  The acquired ability to recognize

and destroy a single disease or
pathogen or its products that do not rely
on previous exposure to a pathogen or
its products.
 The response if you have covid-19 for
the first time
 Cells that participate:
o Dendritic cell
o Macrophages
o Natural killer cell or NKC
o Neutrophils (eusinophil, basophil)
and destroy a particular pathogen
or its products; dependent on
previous exposure to the pathogen
or its products.
 Once antigen is present, adaptive
immunity will came to be
 No adaptive if you haven’t been
infected before
 Cells that participate:
o T cell
o NKC cell
 o Mast cells o B cell – has the antibodies
o T cells o CD8
o CD4

INNATE IMMUNITY

 Also called “in-built ” immunity

 No need for previous exposure to a pathogen
 Mediated by Phagocytes
 Will not be activated without pathogen

1. PATHOGEN - ASSOCIATED MOLECULAR PATTERNS (PAMPs)

 Found Inside or in surfaces of pathogen
 Specific to one pathogen
Examples:
 LPS (Lipopolysaccharide = (fat + sugar) in gram-negative bacteria
 Lipoteichoic acids in gram-positive bacteria (lipids)
 Flagellin – found in flagellated microbes; is a protein
dsRNA of Viruses – can act as pumps (Repeating subunits of a macromolecule)
(e.g. nucleic acid)

2. PATTERN RECOGNITION RECEPTORS (PRR)

 For macrophages
 In macrophages and leukocytes
 The importance of PRR and PAMP:
o recognition to start digestion of the pathogen
 They interact with PAMPs – there is a perfect binding of PRR to the PAMP; when there
is successful binding/recognition, the bacteria will be ingested through phagocytosis
 Initiates digestion of phagocyte to the pathogen
 Without binding of PPR with PAMP, the pathogen will not be recognized; they will
continue to infect the body

ADAPTIVE IMMUNITY

 Also called “antigen-specific immunity” because it relies on the previous exposure

 There is previous exposure to pathogen or its products = Pathogen-specific receptors
 Without pathogen there will be no antigen = no adaptive immunity

HOW ADAPTIVE IMMUNITY IS BEING ACTIVATED

1. The bacteria is engulfed by phagocytosis (goes inside the APC)
2. Antigen from the specific bacteria can now be processed
3. Once processed, they will be presented on the surface of APC
4. MHC II and I act like a hand in presenting the antigen
5. Once there is a presentation of the antigen by the MHC, that will be recognized by T
cells
 2 TYPES OF T CELLS
1. Helper T cell
o Call other immune cell
o It contains T cell receptors
o It only binds with MHC II
o Once there is recognition, it will produce cytokines
 Cytokines – induce inflammation in the specific part of infection

2. Cytotoxic T cell
o They produce perforin granzyme when they have perfect interaction with the
presented antigen by the APC
 Perforin and granzyme – directly kills the antigen bearing cell
o “Cell harboring the antigen”
o It only binds to MHC I

PROCESS

1. Antigen presentation
2. MHC I will hold the Cytotoxic T cell and MHC II will hold the Helper T cell
3. Helper T cell will produce cytokines
4. Other immune cells will rush into a specific site if there is an inflammation

Note:

TCR – holds the T cells (hand for T cell)

MHC – holds the APC (hand for APC)

1. PRIMARY ADAPTIVE IMMUNE RESPONSE

 It is the process replicated by vaccines
 Just starting to recognize the pathogen (kinakapa palang ang antigen); it will create
clone of the antigen reactive cells to understand the pathogens
 Stimulates growth and multiplication of antigen-reactive cells, creating clones
 T cells to T cells receptors (TCRs)
 B cells or antibodies or immunoglobulins
 B cells can differentiate into plasma cells
 Plasma cells – shortlived
o Antibodies – Y shaped structure

2. SECONDARY ADAPTIVE IMMUNE RESPONSE

 Only activated when you are infected with the same pathogen due to the memory cells
 Activates the clones of antigen-reactive cells and generates faster
 May be 10 fold greater than the primary response
o Memory cells – can boost immunity because it can recognize previous antigen;
long-lived cells
 Recognizes the antigen specific to coronavirus
 Stays in the system even after years of recovery
o There are faster production of antibodies in the second infection
             
T cell and Antigen Presentation

❑ Major Histocompatibility Complex (MHC)

▪ MHC I, an antigen presenting molecule found on all nucleated
vertebrate cells
▪ MHC II, an antigen presenting molecule found on APCs only

❑ T lymphocytes
▪ Interact with peptide-MHC complex
▪ Each T cell has TCR
▪ Antigen specific T cells are found in the spleen, lymph nodes and
MALT

o T- cytotoxic (Tc) cells

recognize the antigen presented by an MHC I protein on an
infected cell
Secrete proteins that kill the antigen-bearing cell
o T-helper (TH) cells
interact with peptide–MHC II complexes on the surface of
antigen-presenting cells
Secrete cytokine

Antibodies

❑ Also called immunoglobulins (Igs)

❑ Soluble proteins
❑ Made by B cells and plasma cells
❑ Recognizes specific antigens in the pathogen = kill
❑ B cell will get the antigen from the pathogen to be
presented to T cell
❑ B cells can differentiate to plasma cell or memory cell which can
produce antibodies specific to the previous pathogen

T CELLS AND ANTIGEN PRESENTATION

 Body contains millions of B cells

  located in lymphoid tissue
 each responds to specific antigen
 Become activated in presence of foreign antigen
 unprocessed antigen weak response
 need to process antigen for stronger response
 Unprocessed antigen taken into cell
 incorporated into MHC II self-antigen
 activates helper T cells
 Costimulation- production of cytokines
 Some B cells change into plasma cells
 secrete specific antibodies, at high rate of 4-5 days
 antibodies circulate in lymph and blood to site of invasion
 Circulating antibodies combine w/ antigens
 neutralizes antigen
 immobilizes bacteria
 agglutinating antigens
 activates complement system
 enhances chance antigen will be phagocytized
 Activated B cells
 some turn into memory B cells
 respond more rapidly, forcefully if antigen appears again

NATURAL IMMUNITY

 Natural Active Immunity

 Produced inside of the body
 direct infection
 vaccination
 over time(typically several weeks) to effect
 Acquired through natural infection

 Natural Passive Immunity

 nonimmune person’s acquisition of performed immune cells or antibodies via
natural transfer of cells or antibodies from an immune person
 e.g. (newborn) the antibodies on the breat milk of the mother will be ingested by
the baby and will increase immunity
 mother to baby through the placenta
 immediately to take effect
 Introduced from outside of the body

Artificial Immunity
Immunization
 inoculation of a host with inactive or weakened pathogens or pathogen products to
stimulate protective immunity
a. exposure to a controlled dose of harmless antigen to induce formation of
antibodies (artificial active immunity)
 o e.g. (Vaccines)
b. injecting of antiserum or purified antibodies from an immune individual (artificial
passive immunity)
o e.g. (Donation of plasma)

Immunogen
 also called vaccination
 Developed to create a form of artificial active immunity.
 Inactivated pathogens or their product; killed by chemical agents like phenol or
formaldehyde
 attenuated strains, mutant strain of a pathogen that has lost its virulence but still retains
antigens

Antibiotic Resistance
 Antibiotics

o a chemical compound that a bacterium produces which kills or slows the growth
of a different type of microbe;
o can be extracted from plant materials or can be synthetically produced in the
laboratory
o but most are extracted from bacteria and fungi because they produce secondary
metabolites that can kill pathogens

Examples:
1. Penicillin, Ciprofloxacin resistant Neisseria gonorrhoeae
2. Methicillin Resistant Staphylococcus aureus (MRSA)
3. Extended Spectrum Beta-Lactamase Escherichia coli (ESBL)
o Beta-Lactamase – inhibits Beta Lactam
4. Intrinsic resistance and acquired resistance

 Antibiotic Resistance
o A bacteria's ability to resist antibiotics to which it was previously vulnerable.

 Intrinsic resistance
o The antibiotic cannot inhibit a specific structure is not present in an organism
Example:
Mycoplasma is a bacteria has no cell wall which means that penicillin is
ineffective

 Acquired resistance
o Methicillin-Resistant Staphylococcus Aureus – can be resistant and susceptible
to antibiotics
o MRSA – become resistant to antibiotics because of mecA gene
o

 Susceptible or Sensitive
o Can be killed by the pathogens
MODE OF ACTION OF SOME MAJOR ANTIMICROBIAL AGENTS

 Agents are classified according to their target structures in the bacterial cell. (THF,
tetrahydrofolate; DFH, dihydrofolate; mRNA, messenger RNA)

 Efflux – the ability of bacteria to pump out antibiotics

EXAMPLES OF ANTIBIOTICS
1. Penicillin

o inhibits the cell wall synthesis - inhibits replication of pathogens because they
cannot manufacture their own cell wall
o they undergo replication (synthesis of new strand of DNA) inside the cell
o the newly synthesized DNA will be converted into a single stranded mRNA
(transcription)
o then the mRNA will be used to produce proteins (translation)
o also used for the treatment of gonorrhea
o has a structure called beta-lactam ring
 Ecoli has beta-lactamase enzyme, it can directly change the form of beta-
lactam ring, which makes the penicillin ineffective

 Central dogma of molecular biology (all living things undergo from this)

2. Quinolones

o Target DNA gyrase

o Inhibits DNA replication
 DNA gyrase – enzyme that relaxes the double stranded DNA for DNA
replication

3. Actinomycin

o Stops RNA elongation

o Inhibits transcription
 RNA elongation - a process important for transcription

4. Erythromycin and Tetracyclines

o Inhibits protein synthesis

o Inhibits translation

5. Trimethoprim
o inhibition of metabolism
 o inhibit folic acid metabolism
o the bacteria cannot use folic acid
folic acid – important to produce DNA

PATTERNS OF DRUG RESISTANCE IN PATHOGENS

1. The relationship between antibiotic use and the percentage of antibiotic resistant
bacteria isolated from diarrheal patients
2. Percentage of reported cases of gonorrhea caused by drug resistant strains. Since
1990, penicillin has not been recommended
3. The prevalence of fluoroquinolone-resistant N. gonorrhoeae in certain populations in the
United States in 2003. Ciprofloxacin, a fluoroquinolone, is no longer recommended. We
use Ceftriaxone-cephalosporin today. 

RESISTANCE MECHANISM
 The organism:
1. Lack the structure an antibiotic inhibits.
2. Impermeable to the antibiotic.
3. Able to alter the antibiotic to an inactive form.
4. Modify the target of the antibiotic. Due to mutation in chromosomal genes.
5. Develop a resistant biochemical pathway.
6. Able to pump out an antibiotic entering the cell, a process called efflux.

ANTIBIOTIC RESISTANCE STRATEGIES IN BACTERIA

ANTIMICROBIAL STEWARDSHIP 
-The systematic effort to educate and persuade prescribers of antimicrobials to follow evidence-
based prescribing, in order to stem antibiotic overuse, and thus antimicrobial resistance.
ANTIMICROBIAL STEWARDSHIP:
✓Approach to prevent the emergence of antibiotic
resistance
✓Appropriate selection
✓Dosing
✓Route
✓Duration of antimicrobial therapy

ANTIMICROBIAL STEWARDS:
*Physician
*Pharmacist
*Microbiologist
*Information System Specialist
*Infection Control Professional
*Epidemiologist